NITRIC-OXIDE AS AN AUTOCRINE REGULATOR OF SODIUM CURRENTS IN BARORECEPTOR NEURONS

Arterial baroreceptors are mechanosensitive nerve endings in the aorti c arch and carotid sinus that play a critical role in acute regulation of arterial blood pressure. A previous study has shown that nitric ox ide (NO) or NO-related species suppress action potential discharge of baroreceptors. In the present study, we investigated the effects of NO on Na+ currents of isolated baroreceptor neurons in culture. Exogenou s NO donors inhibited both tetrodotoxin (TTX) -sensitive and -insensit ive Na+ currents. The inhibition was not mediated by cGMP but by NO in teraction with channel thiols. Acute inhibition of NO synthase increas ed the Na+ currents. NO scavengers (hemoglobin and ferrous diethyldith iocarbamate) increased Na+ currents before but not after inhibition of NO synthase. Furthermore, NO production in the neuronal cultures was detected by chemiluminescence and immunoreactivity to the neuronal iso form of NO synthase was identified in fluorescently identified barorec eptor neurons. These results indicate that NO/NO-related species funct ion as autocrine regulators of Na+ currents in baroreceptor neurons. M odulation of Na+ channels may represent a novel response to NO.