<?xml version="1.0" encoding="utf-8"?>
    <rss version="2.0">
      <channel xmlns:content="http://purl.org/rss/1.0/modules/content/">
        <title>Frontiers in Physiology | Vascular Physiology section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physiology/sections/vascular-physiology</link>
        <description>RSS Feed for Vascular Physiology section in the Frontiers in Physiology journal | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-14T07:12:23.662+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1792252</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1792252</link>
        <title><![CDATA[Adrenergic receptors on immune cells in cardiovascular disease: signaling plasticity, biased agonism, and therapeutic opportunities]]></title>
        <pubdate>2026-05-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Laurel A. Grisanti</author><author>Soraya Nekouian</author>
        <description><![CDATA[Sustained sympathetic nervous system activation is a hallmark of hypertension, atherosclerosis, ischemic injury, stroke, and heart failure. While adrenergic receptor (AR) biology is often discussed in cardiomyocytes, vascular smooth muscle, and endothelium, immune cells also express α1-, α2-, and β-ARs, enabling leukocytes to directly sense catecholamine tone and translate it into inflammatory or pro-resolving programs. In this review, we integrate subtype-specific signaling logic (α1AR-Gq/PLC/Ca2+; α2AR-Gi with reduced cAMP; βAR-Gs with cAMP-PKA/EPAC) with key regulatory features that determine outcomes in vivo, including receptor phosphorylation, trafficking and desensitization, compartmentalized signaling, and noncanonical pathways mediated by Gβγ and β-arrestins. We highlight how these mechanisms create context dependence across immune lineages and disease stages, shaping chemotaxis and adhesion, cytokine production, effector functions (for example ROS generation, antigen presentation, and cytotoxicity), and resolution programs such as IL-10-linked responses and efferocytosis. Across CVD contexts, immune cell AR signaling can amplify injury or constrain inflammation, thereby influencing endothelial dysfunction, vascular remodeling, fibrosis, microvascular impairment, and long-term organ function. Finally, we outline translational priorities, including improved mapping of AR expression and signaling states in human immune compartments, immune-phenotyped evaluation of AR-targeted therapies, and precision approaches using subtype-selective or biased ligands to modulate inflammation while preserving essential host defense and repair.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1816892</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1816892</link>
        <title><![CDATA[Unresolved mechanisms: a hypothesized spatial regulation of myosin light chain phosphorylation within the walls of resistance arteries]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Zhe Sun</author><author>Michael A. Hill</author>
        <description><![CDATA[Myosin light chain (MLC) phosphorylation is a fundamental determinant of vascular smooth muscle contraction. While its biochemical regulation has been well-studied, the spatial control of MLC phosphorylation within the vessel wall is less well understood. We recently identified a transmural gradient of phosphorylated MLC (pMLC) across the wall of rat superior cerebellar arteries, with levels peaking in outer-layer (i.e. adventitially directed) vascular smooth muscle cells (VSMCs). This finding suggests that the maintenance of vascular tone may involve spatially heterogeneous contractile signaling at the level of pMLC. We hypothesize that wall tension and consequent mechanotransduction processes to be the primary drivers of this pMLC gradient, potentially through pathways involving adhesion receptors (integrins, N-cadherin), mechanosensitive ion channels, and force-sensitive G protein-coupled receptors in outer-layer VSMCs. In addition, diffusion-limited gradients of endothelium-derived relaxing factors, including nitric oxide and prostacyclin, may establish a counter-gradient of relaxation, strongest at the inner vessel wall. The convergence of these spatially opposing signals—outer-layer mechanotransduction and inner-layer chemical relaxation—conceivably fine-tunes wall tension and stabilizes vascular tone. The proposed hypothesis is generated from evidence supporting this model of spatially regulated MLC phosphorylation as a fundamental mechanism for tension homeostasis in resistance arteries.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1794886</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1794886</link>
        <title><![CDATA[Transcriptomic profiling of the sex-linked biological pathways of severe pulmonary arterial hypertension associated with endothelial cell caveolin-1 depletion and chronic hypoxia]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Joseph W. Leasure</author><author>Samuel M. Lee</author><author>Kayla L. Yerlioglu</author><author>Maricela Castellon</author><author>Haibin Li</author><author>Andrés Fantauzzi</author><author>Sunny Chen</author><author>Sami B. Muslmani</author><author>Arnav Sharma</author><author>Jiwang Chen</author><author>Richard D. Minshall</author>
        <description><![CDATA[IntroductionPulmonary arterial hypertension (PAH) is distinguished by elevated blood pressure and vascular resistance in the arteries of the lungs. Patients with PAH demonstrate pulmonary vascular remodeling, wall thickening, and a high rate of morbidity due to right heart failure. Notably, while female patients are more likely to develop PAH, male patients suffer from higher morbidity rates after diagnosis. The molecular mechanism(s) underlying PAH development is poorly understood, though heritable PAH linked to mutations in bone morphogenic protein receptor 2 (Bmpr2) and caveolin-1 (Cav1) may provide novel insights into the disease’s pathophysiology.MethodsTo interrogate this dynamic, we utilized a global Cav1 knockout (Cav1-KO) mouse model (Cav1-/-) in conjunction with chronic hypoxia to induce symptoms of PAH as demonstrated by hemodynamic and ECHO cardiography recordings.ResultsBoth female and male Cav1-/- mice in chronic hypoxia demonstrated elevated right ventricular systolic pressure (RVSP) of 48.49 mmHg and 47.78 mmHg respectively. Female knockout mice began dying earlier in hypoxic conditions (4 wks), though male mice showed greater total mortality by the end of the 8 wks of hypoxia. In addition to wildtype controls, we compared this knockout mouse to endothelial-specific Cav1 reconstituted (Cav1-RC) knockouts and found that restoration of Cav1 expression only in endothelial cells (ECs) is sufficient to ameliorate PAH symptoms, highlighting the importance of vascular Cav1 in maintaining pulmonary artery function. RNA-sequencing of the lungs revealed that Cav1-/- is associated with downregulation of biological process gene pathways involved in cilium assembly in normoxic conditions for both sexes. In hypoxic conditions, Cav1 knockout in females leads to downregulation of bone morphogenetic protein (BMP) signaling, while male hypoxic Cav1-/- led to a significant increase in muscle cell development genes. Reconstitution of Cav1 in ECs leads to upregulation of immune signaling pathways, muscle cell development, and various cell differentiation pathways in both sexes; females showed a unique upregulation of cilia-related pathways, while males demonstrated increased BMP signaling.DiscussionThese data indicate that muscle cell development, angiogenesis, cilia assembly, immune response, and BMP signaling pathways undergo sex-specific transcriptional regulation during PAH development that may underlie sex differences in PAH patient outcome.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1776903</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1776903</link>
        <title><![CDATA[Science policies and practice of including and excluding women from clinical studies: focus on cardiovascular research]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Anton Kovalsky</author><author>Irena Levitan</author>
        <description><![CDATA[The under-representation of women in clinical studies remains a major issue, recognized by researchers, patients, and legislators alike. In this review, we examine the key legislative documents that have shaped policies governing the exclusion and inclusion of women in clinical research over the past several decades, and their impact on seminal cardiovascular studies. We focus on early federal human-subject regulations codified as the Common Rule, which initially contributed to the near-complete exclusion of women, and trace the gradual recognition of the need for women’s inclusion and the progress achieved to date. Key trials discussed include the Framingham Heart Study, the Multiple Risk Factor Intervention Trial (MRFIT), and the Physicians’ Health Study (PHS), as well as a meta-analysis of over 1, 000 cardiovascular trials conducted between 2017 and 2023. We also discuss the critiques of the legislation including the current reliance on informed consent from a bioethics perspective.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1830278</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1830278</link>
        <title><![CDATA[Sex differences in endothelial cell biology: cellular phenotypes and molecular regulators]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Alexandra Pislaru</author><author>Tara L. Haas</author>
        <description><![CDATA[Endothelial cells (EC) line all blood vessels and are central to maintaining vascular homeostasis by regulating barrier integrity, angiogenesis, inflammation and other key processes. Although EC share core functions, they exhibit substantial heterogeneity across vascular beds and tissues, reflecting differences in local metabolic and microenvironmental conditions. Emerging evidence indicates that endothelial biology is also shaped by sex. Male and female EC differ in multiple aspects of cellular physiology, including metabolic activity, nitric oxide signaling, angiogenic capacity, oxidative stress responses, inflammatory signaling, and susceptibility to senescence. In this review, we summarize the current knowledge of these sex-dependent EC phenotypes and discuss how they vary by vascular location, as well as across age and disease context. Increasing evidence suggests that these differences arise from a complex interplay between sex hormones, sex chromosome complement, epigenetic regulation, and transcription factor networks. We discuss recent advances in understanding these mechanisms and their contributions to EC heterogeneity. Recognizing sex-specific EC functional characteristics and vulnerabilities is critical for a comprehensive understanding of vascular physiology and pathology, with important implications for improved knowledge of vascular disease mechanisms and development of more precise, sex-informed therapeutic strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1811001</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1811001</link>
        <title><![CDATA[Aldosterone increases the expression and subcellular localization of SERCA2a and SERCA2b in the rat mesenteric artery]]></title>
        <pubdate>2026-05-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Cristian J. Arriero-Carrillo</author><author>Hiram Lozano-Ruiz</author><author>Agustín Guerrero-Hernández</author><author>Federico Castro-Muñozledo</author><author>Angélica Rueda</author>
        <description><![CDATA[Aldosterone (Aldo), a mineralocorticoid hormone, modulates cardiovascular function by regulating the expression of intracellular Ca2+ handling proteins, among other effects. In rat resistance-sized mesenteric arteries (MA), Aldo treatment (10 nM, 24 h) upregulates both the L-type voltage-gated Ca2+ channel α1C subunit (CaV1.2) and the Sarco/Endoplasmic Reticulum Ca2+ ATPase (SERCA pump), thereby increasing Sarcoplasmic Reticulum (SR) Ca2+ load. Two SERCA isoforms, SERCA2a and SERCA2b, are expressed in rat MA, but their specific physiological contributions to distinct intracellular Ca2+ signals, remain unclear. In this study, we characterized the relative abundance and subcellular distribution of SERCA2a and SERCA2b in rat MA, their regulation by Aldo, and the impact of Aldo-induced SERCA remodeling on local Ca2+ signals relevant to vascular function, such as Ca2+ sparks and Ca2+ waves. Aldo-treated MA smooth muscle cells (MASMC) exhibited increased Ca2+ spark frequency and a higher incidence of spontaneous Ca2+ waves. Aldo augmented both protein and mRNA levels of SERCA2a and SERCA2b, effects that were blocked by the mineralocorticoid receptor (MR) antagonist RU28318. Under control conditions, SERCA2a was predominantly localized in the perinuclear region, whereas SERCA2b was distributed across both subplasmalemmal and perinuclear regions. Aldo treatment increased the expression of both isoforms in all analyzed subcellular compartments (subplasmalemmal, cytoplasmic, and perinuclear), with a pronounced redistribution towards the subplasmalemmal region of MASMC. This shift in SERCA subcellular distribution likely contributes to enhanced superficial Ca2+ buffering and the ignition of Ca2+ sparks and Ca2+ waves. Furthermore, Aldo increased mRNA levels of mitochondrial transcription factors A and B2 (TFAM and TFB2M), previously implicated in SERCA regulation in human aorta, suggesting a transcriptional mechanism whereby MR activation of the SERCA2 gene is associated with increased TFAM and TFB2M expression. Collectively, these findings demonstrate for the first time that Aldo increases the expression and promotes the subplasmalemmal localization of SERCA2a and SERCA2b in MASMC. This remodeling underscores their critical role in maintaining the superficial Ca2+ buffering system and SR Ca2+ load to prevent pathological elevations in the intracellular Ca2+ concentration. Our results highlight the SERCA pump as a potential therapeutic target in hypertension associated with hyperaldosteronism.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1845969</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1845969</link>
        <title><![CDATA[Editorial: Unraveling the influence of perivascular adipose tissue on vascular health]]></title>
        <pubdate>2026-04-29T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Maria A Delbin</author><author>Stephanie W Watts</author><author>Eduardo Nava</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1757252</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1757252</link>
        <title><![CDATA[A short-term concurrent training program enhances arterial stiffness and flow-mediated dilation in overweight or obese women independent of weight loss]]></title>
        <pubdate>2026-04-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Cristian Álvarez</author><author>Gabriel Rojas</author><author>David C. Andrade</author><author>Pedro Delgado-Floody</author><author>Luis Peñailillo</author><author>Alvaro N. Gurovich</author><author>Mikel Izquierdo</author>
        <description><![CDATA[Background and aimsDespite a wide amount of evidence regarding vascular improvements in overweight/obesity condition, little is known about similar vascular benefits from exercise training without weight loss. This study aimed to evaluate the effects of a 6-week concurrent training (CT) program on pulse wave velocity (PWV), flow-mediated dilation (FMD), and carotid intima-media thickness (cIMT) average (cIMTav) and maximum (cIMTmax) in overweight/obese women who did not report weight loss. Additionally, the relationship between vascular outcomes and anthropometric and body composition measurements was examined.MethodsWe conducted a secondary analysis of a clinical trial assessing the effects of CT on cardiovascular markers. Forty-three overweight/obese women (age = 42.4 ± 12.8 years; BMI = 29.7 ± 3.2 kg/m²) were divided into control (CG, n = 21), ‘exercise without weight loss’ (EG-NWL; n = 9), and ‘exercise with weight loss’ (EG-WL; n = 13) groups. The primary outcomes included PWV, FMD, cIMTav, and cIMTmax, and the secondary outcomes included waist circumference (WC), body fat (BF), skeletal muscle mass (SMM), lean mass, and other vascular measures, reported as absolute and delta (Δ) values.ResultsΔPWV differed between CG and EG-NWL (0.2 vs. –1.2 m·s-1, P = 0.0002) and between CG and EG-WL (0.2 vs. –0.7 m·s-1, P = 0.0002). ΔFMD showed differences between CG and EG-NWL (–0.6 vs. 6.9%) and between CG and EG-WL (–0.6 vs. 4.5%). Each delta of ΔPWV, ΔFMD, ΔcIMTav, and ΔcIMTmax was significantly associated with ΔWC (rs = 0.920; 0.912; 0.597; 0.767, P < 0.05), ΔBF% (rs = 0.847; 0.791; 0.465; 0.695, P < 0.05), ΔSMM (rs = 0.889; 0.566; 0.934; 0.940, P < 0.05).ConclusionOverweight and obese women who did not lose weight after CT experienced a decrease in PWV and an increase in FMD. The correlations between changes in ΔPWV, ΔFMD, ΔcIMTav, and ΔcIMTmax with body composition measures suggest directions for future research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1778955</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1778955</link>
        <title><![CDATA[In vitro evidence that plasma of women with eclampsia disrupts the blood-brain barrier]]></title>
        <pubdate>2026-04-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jesenia Acurio</author><author>Felipe Troncoso</author><author>Esthefanny Escudero-Guevara</author><author>Hermes Sandoval</author><author>Belen Ibañez</author><author>Manu Vatish</author><author>Pablo Torres-Vergara</author><author>Lina Bergman</author><author>Carlos Escudero</author>
        <description><![CDATA[BackgroundEclampsia is a severe complication of preeclampsia involving blood-brain barrier (BBB) disruption. While small extracellular vesicles (sEVs) contribute to endothelial dysfunction in preeclampsia, their role in eclampsia remains unclear. We examined the effects of plasma and plasma-derived sEVs from women with eclampsia on BBB integrity.MethodsPlasma and plasma-sEVs were isolated from women with normotensive pregnancies (n=18), preeclampsia (n=19), preeclampsia with organ complications (n=17), and eclampsia (n=20). An in vitro BBB model based on the culture of human brain endothelial cells was used to evaluate electrical resistance (TEER) and Dextran 70 kDa permeability in the presence of women’s plasmas or plasma-sEVs. sEVs cargo of relevant proteins involved in BBB regulation, eNOS, and TNF-α, were analyzed.ResultsPlasma from women with eclampsia disrupted the BBB, with marked reductions in TEER and increased permeability compared to normotensive controls, preeclampsia, and preeclampsia with organ complications. Moreover, plasma-sEVs of women with eclampsia caused a drop in TEERs but less BBB permeability than plasma-sEVs from normotensive controls or preeclampsia. Lower levels of eNOS and TNF-α in eclampsia-derived sEVs compared to normotensive controls were found.ConclusionsWe report the critical role of circulating plasma factors in the disruption of the BBB during eclampsia. Although plasma-derived sEVs induce some alterations in barrier properties, our findings suggest they are not the main drivers of the BBB impairment observed in eclampsia, likely due to altered cargo composition.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1796673</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1796673</link>
        <title><![CDATA[Preeclampsia as an early manifestation of cardiovascular–kidney–metabolic syndrome]]></title>
        <pubdate>2026-04-14T00:00:00Z</pubdate>
        <category>Opinion</category>
        <author>Priscila Oliveira Barbosa</author><author>Luiz Sérgio Lima-Junior</author><author>Ricardo Carvalho Cavalli</author><author>Gizele Celante</author><author>Roberto da Silva Gomes</author><author>Valeria Cristina Sandrim</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1801670</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1801670</link>
        <title><![CDATA[NO- and S-nitrosothiols-dependent relaxation in large and small resistance blood vessels]]></title>
        <pubdate>2026-04-13T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Mauricio A. Lillo</author><author>Annie Beuve</author>
        <description><![CDATA[Nitric oxide (NO) has long been viewed as the principal endothelium-derived vasodilator through activation of soluble guanylyl cyclase (GC1) and cGMP-dependent signaling in vascular smooth muscle. However, accumulating evidence indicates that this canonical NO-GC1-cGMP pathway predominates in large conduit arteries, whereas regulation of vascular tone and blood pressure in the microcirculation relies largely on endothelium-derived hyperpolarization (EDH) with NO acting primarily as a redox signal rather than a freely diffusing gas. Here, we review emerging mechanisms that integrate NO-derived nitrosative signaling with EDH, highlighting the central role of protein S-nitrosation and transnitrosation in shaping endothelial excitability. A central focus of this review is the newly-identified endothelial role of GC1 beyond its canonical smooth muscle function. We summarize recent findings demonstrating that GC1 acts as a redox hub through S-nitrosation of a critical cysteine residue (cys), enabling selective transnitrosation of downstream targets that regulates endothelial Ca2+ influx, KCa channel activation, and EDH-dependent vasodilation independently of cGMP production. Finally, we examine how extravascular components-including perivascular adipose tissue and red blood cells-modulate EDH signaling under physiological and pathological conditions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1741037</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1741037</link>
        <title><![CDATA[Nuclei isolation from rat and cow white adipose tissues for single-nucleus RNA sequencing; rat WAT remains a challenge]]></title>
        <pubdate>2026-03-26T00:00:00Z</pubdate>
        <category>Methods</category>
        <author>Janice M. Thompson</author><author>Miguel Chirivi</author><author>Leah Terrian</author><author>G. Andres Contreras</author><author>Stephanie W. Watts</author><author>Rance Nault</author>
        <description><![CDATA[Perivascular adipose tissue (PVAT) is a complex tissue that is increasingly recognized for its roles in vascular health and disease. The form and function of PVAT are different depending on species and anatomical location, and understanding its cellular and molecular characteristics gives greater insights. We had previously successfully performed single-nucleus RNA sequencing (snRNAseq) on brown fat depots, the thoracic aortic PVAT (taPVAT) and subscapular brown adipose tissue (BAT), from Dahl Salt Sensitive rats. However, the application of the same nuclei isolation method to white adipose tissue (WAT) depots (perivascular and non-perivascular) from the same rat strain resulted in insufficient nuclei capture and low transcript numbers. These challenges were also encountered when processing WAT from cattle. While nuclei isolation methods have been developed and optimized for human and mouse WAT depots, they have not been evaluated across WAT depots from other species, such as cow and rat. Because these latter species are important models for cardiovascular and metabolic diseases, this study aimed to validate and optimize a nuclei isolation protocol for use with WAT from them. Protocols were evaluated based on a) the quantity of nuclei isolated, b) the quality of nuclei determined via microscopic visualization, and c) the total number of detected transcripts and genes following snRNAseq. A modified protocol developed for human WAT, incorporating liquid nitrogen pulverization and Dounce homogenization of flash-frozen tissue, was tested. This protocol, with key modifications for optimization, proved translatable to rat and cow WAT depots to improve nuclei yield (rat retroperitoneal fat, 3,100 nuclei/mg tissue; rat mesenteric perivascular adipose tissue, 2,200 nuclei/mg tissue; cow white fat, 2,050 nuclei/mg tissue). Further analysis via snRNAseq, however, identified limitations. While cow WAT expressed nearly 1,720 median genes/cell, both rat white depots were significantly lower [mesenteric PVAT (mesPVAT), 189; retroperitoneal (RP) fat, 294 median genes/cell], hindering downstream analyses in the rat tissue. These findings suggest that biological differences in adipose depots within and between species pose important challenges for the application of snRNAseq on rat WAT.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1802411</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1802411</link>
        <title><![CDATA[Sex differences in arterial stiffness in a rat model of type 1 diabetes]]></title>
        <pubdate>2026-03-20T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Swasti Rastogi</author><author>Amanda A. de Oliviera</author><author>Yingnan Zhai</author><author>Jessica Liaw</author><author>Linxia Gu</author><author>Kenia P. Nunes</author>
        <description><![CDATA[BackgroundIndividuals with type 1 diabetes (T1D) exhibit elevated arterial stiffness and are at a higher risk of developing cardiovascular disease, both of which are sex dependent. However, whether sex differentially affects aortic structure at macro-, micro-, and nano-levels, which represent evaluations of the aorta at multiple scales, remains poorly understood. Therefore, we investigated sex-based differences in arterial stiffness by assessing pulse wave velocity (PWV), extracellular matrix remodeling, and atomic force microscopy (AFM) based medial-layer biomechanics in the aorta of a rat model of T1D.MethodsMale and female Sprague Dawley rats were injected intraperitoneally with streptozotocin (65 mg/kg) to induce T1D. After 4 weeks, arterial stiffness and vascular alterations were evaluated in aortas of both sexes across multiple levels. At the macro-level, in vivo arterial stiffness was measured using ultrasound-based PWV. At the micro-level, structural remodeling was evaluated by quantifying collagen and elastin content in the aortic extracellular matrix. At the nano-level, biomechanical properties were assessed using AFM to determine Young’s modulus in the aortic tissue.ResultsT1D increased in vivo PWV in both sexes, with significantly higher PWV in diabetic males compared to diabetic females. Structural analysis revealed that diabetic males exhibited higher collagen deposition than diabetic females, whereas the Young’s modulus increased with diabetes but showed no differences associated with sex.DiscussionThese findings suggest that sex differences in T1D-related arterial stiffness at the macro level are primarily associated with extracellular matrix remodeling rather than nanoscale vascular smooth muscle cell stiffness at this disease stage.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1777457</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1777457</link>
        <title><![CDATA[Imaging photoplethysmography reveals differences in the reactions of cerebral and systemic hemodynamics to infusion of vasoactive drugs]]></title>
        <pubdate>2026-03-19T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Alexey Y. Sokolov</author><author>Valeriy V. Zaytsev</author><author>Anton V. Shcherbinin</author><author>Alexei A. Kamshilin</author>
        <description><![CDATA[IntroductionAccording to the recent data, imaging photoplethysmography has extensive capabilities in clinical and experimental biomedical research. However, relationship between local vasomotor reactions, estimated as fluctuations of the amplitude of pulsatile component (APC) of a photoplethysmographic waveform, and changes in systemic hemodynamic parameters remains unclear. The study aims to assess APC changes concurrently with changes in basic physiological parameters in response to administration of either vasodilating adenosine triphosphate or vasoconstrictor norepinephrine.MethodsIn anesthetized, artificially ventilated rats (n=10), a video recording of the cerebral cortex was performed through thinned parietal bones synchronously with an electrocardiogram. Simultaneously, systemic blood pressure and end-tidal CO2 were monitored.ResultsCerebrovascular effects of vasoactive agents are expressed in transient, pronounced and stereotypical changes in APC for all animals. For both substances, these changes are multiphasic, with at least two episodes of rise and fall in APC that do not correlate with changes in blood pressure. For the first time, opposite reaction vectors of intracranial and systemic hemodynamics were detected with the administration of either vasodilators and vasoconstrictors.DiscussionOur study demonstrates that APC can be considered as a quantitative marker of local vasodilation/vasoconstriction, which does not necessarily coincide with systemic hemodynamics, thus enabling an experimental investigation of autoregulation processes. The results obtained make it possible to link systemic and intracranial hemodynamic shifts caused by drugs into a single picture and clarify how adenosine triphosphate or norepinephrine affect the cardiovascular system and blood supply to the brain, which is very important due to the widespread use of these drugs in practical medicine.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1739696</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1739696</link>
        <title><![CDATA[Vascular, physical fitness, lifestyle, and body composition characteristics in middle-aged and older diver fishermen: association between shear rate and lower-limb physical fitness]]></title>
        <pubdate>2026-03-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Alex Véliz</author><author>Raquel Pereira Berríos</author><author>Anita Dörner Paris</author><author>David C. Andrade</author><author>Cristian Álvarez</author>
        <description><![CDATA[ObjectivesFirst, to describe the vascular, physical fitness, lifestyle, and body composition characteristics of middle-aged and older adult diver fishermen. Second, to associate vascular outcomes with physical fitness (upper and lower limbs).MethodsA descriptive pilot study was performed in middle-aged [MA-DF, n = 11, body mass index (BMI) 29.9 ± 4.9, mean arterial pressure (MAP) 103.9 ± 6.2 mmHg] and older (OA-DF, n = 11, BMI 28.5 ± 2.7, MAP 111.8 ± 9.6 mmHg) adult diver fishermen. In each group, brachial (BA) and common carotid artery (CCA) diameter (DBA; DCCA), peak systolic (PSVBA; PSVCCA), end-diastolic velocity (EDVBA; EDVCCA), shear rate (SRBA; SRCCA), resistance index (RIBA; RICCA), pulsatility index (PIBA; PICCA), Reynolds number (ReBA; ReCCA), handgrip strength right (HGSRA), left (HGSLA), and average (HGSAV) and lower-limb fitness (Ruffier test) were the main outcomes, while other types of information, including vascular ankle-brachial index, pulse wave velocity, carotid intima average and maximum, augmentation index, body composition (segmental and total parameters by dual-X-ray absorptiometry), and lifestyle, were secondary outcomes.ResultsThere were no vascular, body composition, or lifestyle differences between groups. The MA-DF group showed superior upper- (HGSRA 48.1 ± 6.2 kg vs. 39.8 ± 6.4 kg; HGSLA 46.7 ± 5.9 kg vs. 39.5 ± 6.3 kg, both P < 0.05) and lower-limb fitness (Ruffier test 23.2 ± 5.3 repetitions vs. 15.5 ± 2.4 repetitions, p = 0.0006) vs. the OA-DF group. Significant associations were found between SRBA and the Ruffier test (p = 0.003) and between SRCCA and the Ruffier test (p = 0.042).ConclusionDespite similar vascular, lifestyle, and body composition profiles, middle-aged and older diver fishermen displayed marked differences in upper- and lower-limb physical fitness. Importantly, lower-limb physical fitness, as assessed by the Ruffier test, emerged as a robust correlation of vascular shear rate (SR) in both the BA and CCA, highlighting its potential relevance to peripheral and central vascular function.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1754344</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1754344</link>
        <title><![CDATA[Sex-specific modulation of T-type voltage-gated calcium channels in the renal artery of hypertensive rats]]></title>
        <pubdate>2026-03-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Andrea Suarez</author><author>Sol Guerra-Ojeda</author><author>Alicia Valls</author><author>David Verdú</author><author>Marta Serna-García</author><author>Guadalupe Herrera</author><author>Eva Serna</author><author>Maria D. Mauricio</author>
        <description><![CDATA[IntroductionHypertension contributes to cardiovascular disease, with growing evidence of sex-specific differences in its underlying mechanisms. T-type voltage-gated calcium channels (VGCCs) have emerged as key regulators of vascular tone, particularly under conditions of nitric oxide (NO) deficiency. However, their role in mediating vascular dysfunction across sexes remains poorly understood.MethodsThis study examined the role of T-type VGCCs and their modulation by NO in the renal artery of male and female spontaneously hypertensive rats (SHR). Vascular reactivity was assessed through phenylephrine-induced contractions in the presence or absence of nickel chloride (NiCl2), a T-type VGCC blocker, and L-NAME, an inhibitor of nitric oxide synthase (NOS). Gene expression of T-type VGCCs (CaV3.1 and CaV3.2) and eNOS was quantified by RT-PCR. Oxidative stress parameters in leukocytes were assessed by flow cytometry to explore the systemic redox.ResultsHypertension induced a rightward shift of the acetylcholine-mediated vasorelaxation curve. In male rats, hypertension did not significantly alter the phenylephrine concentration-response curve. A single data point showed a significant difference following incubation with L-NAME. The contribution of T-type VGCCs to vascular reactivity remained unchanged. Male SHRs displayed increased mRNA expression of CaV3.1, CaV3.2, and eNOS, yet showed no corresponding increase in T-type VGCC activity or NO availability. Conversely, in female SHR, phenylephrine concentration-response curve showed a leftward shift, reduced NO release, and increased participation of T-type VGCCs in response to phenylephrine. Furthermore, pharmacological inhibition of NO synthesis in female WKY rats, used to simulate hypertensive conditions, enhanced the involvement of T-type VGCCs in phenylephrine-induced vasoconstriction. mRNA expression of eNOS was not modified by hypertension in females. Despite the heightened T-type VGCCs activity, female SHRs had reduced mRNA expression of CaV3.1 and CaV3.2, suggesting a potential compensatory downregulation. Finally, leukocytes of male SHR exhibited significantly increased production of H2O2 and ONOO− compared to the other studied groups, suggesting that hypertension contributes to a greater oxidative stress in male.DiscussionThese findings reveal sex-specific differences in the role of T-type VGCCs during hypertension and underscore the therapeutic potential of targeting T-type VGCCs, particularly in females, as a sex-specific strategy for more effective and personalized hypertension management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1693470</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1693470</link>
        <title><![CDATA[Cardiovascular risk and obesity in miner workers exposed to intermittent hypobaric hypoxia in the Peruvian Andes]]></title>
        <pubdate>2026-03-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Elizbet S. Montes-Madariaga</author><author>Brando Ortiz-Saavedra</author><author>Julio S. Mamani-Castillo</author><author>Anel Ivonne Valencia-Pacheco</author><author>Brenda Oporto-Arenas</author><author>Jose Luis Manrique-Ccopa</author><author>Jorge Ballón-Echegaray</author><author>Irmia Paz</author><author>Ricardo David Davila Ralaiza</author><author>Arturo A. Arce-Esquivel</author><author>Oscar Moreno-Loaiza</author><author>Ricardo A. J. Leon-Vasquez</author>
        <description><![CDATA[BackgroundOccupational activities such as mining and interprovincial transportation expose Peruvian workers to large altitude fluctuations, generating repeated cycles of chronic intermittent hypobaric hypoxia (CIHH). In this study, we aimed to evaluate the effect of CIHH exposure on cardiovascular risk, obesity, sleep quality, and physical activity among male workers performing rotational shifts at high altitude.MethodsA cross-sectional study was conducted with 96 male participants aged 20–60 years, who were divided into two groups: those exposed to CIHH (n = 53; ≥3,000 m, alternating with <2,500 m) and controls working permanently at low altitude (<2,500 m; n = 43). Anthropometric and body composition parameters were assessed by bioelectrical impedance, and cardiovascular risk was estimated using the Reynolds Risk Score (RRS) and Framingham Risk Score (FRS). Sleep apnea risk and physical activity were evaluated using the STOP-Bang Questionnaire and the International Physical Activity Questionnaire—Short Form (IPAQ-SF), respectively. Biochemical and hematological profiles were also analyzed.ResultsObesity prevalence was significantly higher in the CIHH group (80%) than in controls (20%) (p = 0.036; PR = 1.58, 95% CI: 1.12–2.24). Despite this, body fat (56.8% vs. 43.2%, p = 0.5), skeletal muscle (55.2% vs. 44.8%, p = 0.9), and visceral fat (57.8% vs. 51.0%, p = 0.5) did not differ significantly. Hematocrit levels were higher in CIHH workers (median 52.3%) than in controls (50.7%) (p = 0.03), indicating mild erythropoietic adaptation. No significant between-group differences were observed in lipid profile, glucose, insulin, high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), physical activity, or obstructive sleep apnea (OSA) risk (all p > 0.05). Estimated cardiovascular risk remained low and comparable between groups.ConclusionCIHH exposure was associated with higher hematocrit levels and a significantly greater prevalence of obesity but no adverse alterations in cardiovascular or metabolic biomarkers. These findings suggest a dual physiological response to intermittent hypoxia—erythropoietic adaptation coexisting with metabolic vulnerability—highlighting the need for preventive strategies in high-altitude occupational health.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1773582</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1773582</link>
        <title><![CDATA[Acute effect of citrulline malate on flow-mediated dilation and serum pharmacodynamics in healthy young males]]></title>
        <pubdate>2026-03-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Johan Grannes</author><author>Nigel A. Callender</author><author>Adam M. Gonzalez</author><author>Jonny Hisdal</author><author>Fredrik T. Vårvik</author><author>Thomas Bjørnsen</author>
        <description><![CDATA[IntroductionThe use of ergogenic compounds has gained increasing popularity among individuals who wish to improve performance and recover faster from their workouts. Among these products is citrulline malate (CitMal), a popular dietary supplement that is suggested to enhance nitric oxide (NO)-mediated vasodilation and muscle blood flow.MethodsTo evaluate effects on arterial function, flow-mediated dilation (FMD) of the brachial artery during active hyperemia was measured in 12 healthy, recreationally active males (23 ± 3 years) before and after (60- and 120-min post) consuming either 6 g CitMal, 12 g CitMal, or a taste-matched placebo. The study used a randomized, double-blind, placebo-controlled, within-subject counterbalanced crossover design with ≥7-day washouts.ResultsRepeated measures ANOVA revealed no significant interaction (p = 0.315) or time effect (p = 0.649) in corrected FMD% at 60- and 120-min after intake of placebo, 6 g CitMal, and 12 g CitMal. There were also no significant differences (p = 0.301) between doses at any timepoint. A subgroup of six participants completed two additional visits to assess the effect of CitMal ingestion on serum markers involved in NO production. Over 120-min post-consumption, both doses significantly increased peak serum concentrations of citrulline (6 g: 504.7 ± 139.7; 12 g: 881.9 ± 216.7 μM), arginine (6 g: 70.2 ± 20.4; 12 g: 101.8 ± 36.2 μM), and ornithine (6 g: 27.9 ± 14.2; 12 g: 56.5 ± 30.0 μM) from baseline (all p < 0.001), with greater increases following 12 g (all p < 0.05). Likewise, arginine-to-dimethylarginine ratios (SDMA and ADMA) increased from baseline (SDMA, 6 g: 114.1 ± 24.2; 12 g: 166.2 ± 43.7; ADMA, 6 g: 119.2 ± 31.8; 12 g: 169.1 ± 29.1; all p < 0.001), with greater increases following 12 g (p < 0.05).DiscussionCollectively, these findings suggest that neither 6 g nor 12 g of CitMal significantly enhance FMD within 120 min, despite marked increases in biochemical markers favorable to NO production. To our knowledge, this is the first study to compare acute doses of CitMal up to 12 g in relation to brachial artery FMD. These results indicate that acute vascular responses to CitMal may be limited by physiological ceiling effects and that potential vascular benefits may depend on longer-term supplementation, the presence of an exercise stimulus, or populations with impaired endothelial function.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1728065</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1728065</link>
        <title><![CDATA[Neurovascular coupling and cerebrovascular reactivity: physiology, lifespan development, pathophysiology, and clinical relevance]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Zena Khartabil</author><author>David Kala</author><author>Yeva Prysiazhniuk</author><author>Jakub Otáhal</author>
        <description><![CDATA[Neurovascular coupling (NVC) and cerebrovascular reactivity (CVR) are two key regulatory mechanisms that maintain adequate cerebral blood flow (CBF) to meet the metabolic demands of the human brain. In this review, we summarize the essential physiological principles needed to understand the distinctions, similarities, and overlaps between these systems, providing a deeper comprehension of cerebral perfusion and its regulation. We further examine their development across the lifespan, including embryogenesis and early life, with a focus on how synaptogenesis, myelination, and synaptic pruning shape NVC, CVR, and CBF. Finally, we discuss the effects of aging, emphasizing cerebrovascular remodeling and its consequences. Various neuropathologies are then explored from the perspective of altered CBF regulation, highlighting numerous correlations between regulatory dysfunction and disease pathogenesis. We also review a range of investigative techniques used to assess NVC and CVR, including (but not limited to) arterial spin labelling, functional magnetic resonance imaging, and transcranial Doppler. This review systematically integrates the developmental trajectories of NVC and CVR across the human lifespan with their pathophysiological alterations and clinical assessment methods. By combining developmental, mechanistic, and clinical perspectives, it provides a comprehensive framework that highlights how age-related changes shape cerebrovascular regulation, with important implications for both research and the interpretation of neurovascular data.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1704443</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1704443</link>
        <title><![CDATA[Single-cell transcriptomics reveals heterogeneous neutrophil populations and diagnostic biomarkers in atherosclerosis]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ping Wang</author><author>Qiang Fu</author><author>Yuefeng Cai</author><author>Jiaxin Yang</author><author>Zhenzhen Cui</author><author>Qiyu Sun</author><author>Quanli Qiu</author><author>Xiaowen Ma</author><author>Min Li</author>
        <description><![CDATA[IntroductionAtherosclerosis, a chronic inflammatory arterial disease, involves complex interactions among diverse immune cells. Although single-cell RNA sequencing (scRNA-seq) has revealed cellular heterogeneity within atherosclerotic lesions, the diversity of neutrophils and their crucial genes in atherogenesis remain elusive.MethodsWe integrated scRNA-seq data from six human atherosclerotic samples, comprising 47,604 single cells.The Harmony algorithm was applied for dimensionality reduction and batch effect correction, resulting in the identification of 16 distinct cell subtypes. High-resolution weighted gene co-expression network (hdWGCNA) analysis was performed to construct a gene co-expression network specifically within the neutrophil subtype. Characteristic genes were selected using Lasso regression. Immune infiltration analysis, gene set enrichment analysis (GSEA), and gene set variation analysis (GSVA) were conducted to investigate the biological functions and potential regulatory mechanisms of the key genes. An atherosclerosis animal model was employed to validate the expression levels of the key genes in carotid artery tissues. In addition, transcriptional regulatory network analysis and correlation analysis between key genes and atherosclerosis-related regulatory genes were carried out. Drug prediction was performed using the Connectivity Map (CMap) database.ResultsA total of 16 cell subtypes were identified following batch effect correction. Annotation results revealed a increased proportion of neutrophils in atherosclerotic arteries compared to healthy controls. WGCNA analysis of neutrophil subtypes unveiled four key genes: CSTB, CHST15, RNASE1 and ATP2B1, which were validated as promising candidate biomarkers in independent cohorts (AUC >0.85). Preliminary validation in the animal model showed that the expression levels of the four genes were elevated in diseased carotid artery tissues compared to normal controls. Immune infiltration analysis demonstrated significant correlations between the key genes and the infiltration levels of multiple immune cell types. GSEA and GSVA showed that these genes were primarily enriched in pathways associated with inflammatory response, ferroptosis, and atherosclerosis-related signaling pathways. Transcriptional regulation analysis predicted potential transcription factors, and correlation analysis revealed significant associations between the key genes and known atherosclerosis-related regulatory genes. CMap analysis predicted several small-molecule compounds with potential therapeutic effects.DiscussionOur findings uncover the previously unrecognized heterogeneity of neutrophils in atherosclerosis and identify four key genes as promising diagnostic markers and therapeutic targets. These findings provide new insights into the pathogenesis of atherosclerosis and provide a theoretical basis for developing targeted therapies against this devastating disease.]]></description>
      </item>
      </channel>
    </rss>