ADENOSINE-TRIPHOSPHATE ATTENUATES RENAL SYMPATHETIC-NERVE ACTIVITY THROUGH LEFT-VENTRICULAR CHEMOSENSITIVE RECEPTORS

We previously reported that ATP, but not adenosine, administered i.v. attenuates the baroreflex-mediated increase in sympathetic nerve activ ity in response to arterial hypotension by a vagal afferent mechanism. It was not elucidated in that study which vagal afferent endings are involved. Mongrel dogs were anesthetized with alpha-chloralose, thorac otomy was performed and a 27-gauge hypodermic needle was inserted into the left circumflex coronary artery. The left renal sympathetic nerve s were isolated and placed on a bipolar silver electrode for measureme nt of renal sympathetic nerve activity (RSNA). Dose-response effects o f intracoronary or i.v. infusion of ATP (100, 200 or 400 mu g/kg/min) on RSNA and mean arterial pressure were studied in neuraxis-intact and cervically vagotomized dogs. RSNA was increased dose-dependently with decreasing mean arterial pressure during the i.v. ATP infusion. Eleva tion of RSNA was attenuated by higher intracoronary ATP infusion rates , despite the fact that mean arterial pressure was decreased dose-depe ndently. Left ventricular end-diastolic pressure, however, remained un changed. This suppression of RSNA by the intracoronary ATP infusion wa s completely abolished by bilateral cervical vagotomy. Our data sugges t that ATP attenuates reflex increases in sympathetic nerve activity b y possibly stimulating ventricular chemoreceptors with cardiac vagal a fferents.