Ionic sensitivity of baroreceptors.

Baroreceptors respond to distortion of their receptor regions by producing action potentials and, thus, provide information to the central nervous system for cardiovascular control. The mechanisms converting mechanical events to electrical signals are unknown. Since it has not been possible to record a receptor potential in the mechanosensitive terminals, studies rely on interpretation of axonal discharge of baroreceptor endings. In the present study, the ionic sensitivity of in vitro preparations of both low- and high-pressure receptors are compared in studies in which the ionic composition of the extracellular fluid is controlled. The results taken together with previous work suggest uniformity of response to calcium, sodium, and potassium across a variety of cardiovascular receptor types supporting common mechanoelectrical transduction mechanisms. Decreased extracellular sodium produced increased threshold and decreased slopes of pressure-discharge curves for both aortic arch baroreceptors and for low-pressure baroreceptors in the atrium. Results are consistent with data for other mechanoreceptors where it is believed that distortion activates a relatively poorly selective cation-conducting channel through the membrane. As with arterial baroreceptors, increases in external calcium levels caused a decrease in the excitability of atrial baroreceptors. Substitution of half the external calcium with the inorganic calcium channel blocker cobalt failed to alter baroreceptor function. Bay K 8644, a calcium channel agonist of the dihydropyridine class of calcium channel blockers, tended to inhibit baroreceptor discharge with effects consistent with smooth muscle activation within the vessel wall. Several hypotheses of potential underlying mechanisms are discussed. These new experiments are consistent with the results achieved with alterations of ionic calcium and suggest that calcium entry does not play a detectable role in baroreceptor transduction.