MECHANOSENSITIVE POTASSIUM CHANNELS IN NEURONS WITH CARDIAC AXONS OF THE NODOSE GANGLION IN RATS

Peter Linz¹Eva Hutter¹Tilmann Ditting^1,2Mario Schiffer¹Kerstin Amann³Karl F. Hilgers¹Roland Veelken^1*Kristina Rodionova¹

• ¹Universitatsklinikum Erlangen Medizinische Klinik 4 Nephrologie und Hypertensiologie, Erlangen, Germany
• ²Klinikum Nurnberg, Nuremberg, Germany
• ³Universitätsklinikum Erlangen, Nephropathologie, Erlangen, Germany

Cardiac vagal afferent neurons located in the nodose ganglion play a pivotal role in cardiopulmonary reflexes that couple cardiac filling states to renal sympathetic outflow and circulatory homeostasis. Their excitability depends on a fine balance of depolarizing and repolarizing ion fluxes, yet the contribution of mechanosensitive ion channels to this regulation remains incompletely understood. While non-selective cation channels such as Piezo1/2 are established mediators of baroreceptor function, they are not directly responsible for repolarization. In contrast, mechanosensitive potassium channels are ideally suited to terminate action potentials and thereby shape afferent signaling from the heart. We therefore tested the hypothesis that mechanosensitive (MS) potassium channels are functionally expressed in nodose ganglion neurons with cardiac projections. Using excised-patch recordings with stepwise suction, we identified two types of MS channels. One was inhibited by extracellular gadolinium (100 µM) and exhibited a higher unitary conductance, while the other was insensitive to gadolinium and showed a lower conductance. Both channel types were predominantly selective for K⁺ but also permeable to Na⁺, with a relative K⁺: Na⁺ permeability of ~3.3–3.4. This mixed selectivity provides sufficient depolarization to activate voltage-gated Na⁺ channels and thereby initiate action potential firing. Our findings provide direct evidence for the presence of MS potassium channels in cardiac vagal afferent neurons and suggest that they may contribute critically to mechano-electric coupling and reflex control of cardiovascular function.