AUTHOR=Berg Torill 

TITLE=β- and α2-Adrenoceptor Control of Vascular Tension and Catecholamine Release in Female Normotensive and Spontaneously Hypertensive Rats

JOURNAL=Frontiers in Neurology

VOLUME=8

YEAR=2017

URL=https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2017.00130

DOI=10.3389/fneur.2017.00130

ISSN=1664-2295

ABSTRACT=<p>As in humans, young, female, spontaneously hypertensive rats (SHR) have a lower blood pressure than male SHR. In male, normotensive rats (WKY), α<sub>2</sub>- and β<sub>1+2</sub>-adrenoceptors (AR) reciprocally controlled catecholamine release and vascular smooth muscle tension. This interaction was malfunctioning in male SHR. The present study analyzed if a favorable shift in the α<sub>2</sub>/β<sub>1+2</sub>AR interaction may represent an antihypertensive protection in females. Female SHR (early hypertension, 12–14 weeks) and age-matched WKY were infused with tyramine (15 min) to stimulate norepinephrine (NE) release through the reuptake transporter, consequently preventing reuptake. Presynaptic control of vesicular release was therefore reflected as differences in overflow to plasma. The released NE increased total peripheral vascular resistance (TPR). The results showed that β<sub>1&gt;2</sub>AR facilitated tyramine-stimulated NE release in both strains, also in the presence of α<sub>2</sub>AR-antagonist (L-659,066). βAR-antagonist (atenolol-β<sub>1</sub>, ICI-118551-β<sub>2</sub>, nadolol-β<sub>1+2</sub>) had no effect on the increased secretion of epinephrine after L-659,066 in WKY, but β<sub>1&gt;2</sub>AR-antagonist augmented the L-659,066-induced increase in the secretion of epinephrine in SHR. Nadolol increased the TPR response to tyramine with a greater effect in WKY than SHR, whereas β<sub>1or2</sub>-selective antagonists did not. One βAR-subtype may therefore substitute for the other. When both β<sub>1+2</sub>AR were blocked, α<sub>2</sub>AR-antagonist still reduced the TPR response in WKY but not SHR. Thus, α<sub>2</sub>/β<sub>1+2</sub>AR reciprocally controlled catecholamine release, with a particular negative β<sub>1</sub>AR-influence on α<sub>2</sub>AR-auto-inhibition of epinephrine secretion in SHR. Moreover, in these female rats, β<sub>1/2</sub>AR-independent α<sub>2</sub>AR-mediated vasoconstriction was seen in WKY but not SHR, but β<sub>1/2</sub>AR-mediated vasodilation downregulated adrenergic vasoconstriction, not only in WKY but also in SHR.</p>