Excitation of cardiac sympathetic afferent nerves: effects on renal function.
Cardiac sympathetic afferent nerves can reflexly alter renal efferent nerve activity during myocardial ischemia and in response to mechanical or chemical stimulation of cardiac receptors. They also may influence renal excretion of water and electrolytes; however, this potential influence on renal function has not been determined. Therefore, receptors of cardiac sympathetic afferent nerves were chemically stimulated by epicardial application of bradykinin to determine effects on renal function. Experiments were performed in anesthetized dogs in which cervical vagosympathetic trunks were severed and common carotid arteries were tied to diminish influences of arterial baroreceptors and vagal afferent nerves. Chemical stimulation of cardiac afferent neurons excited renal nerve activity and produced decreases in urine flow rate, glomerular filtration rate, and excretion of sodium and potassium. In contrast, no consistent changes in renal function were observed in control dogs, which did not undergo cardiac afferent stimulation. These data provide evidence that activation of cardiac sympathetic afferent neurons can lead to alterations in excretion of water and electrolytes as well as changes in renal nerve activity.
D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D001920:Bradykinin / Q000494:pharmacology; D004285:Dogs; D005260:Female; D006321:Heart / Q000294:innervation*; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D008297:Male; D011188:Potassium / Q000378:metabolism; D011311:Pressoreceptors / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology
D012964:Sodium; D011188:Potassium; D001920:Bradykinin