Contrasting reflexes evoked by chemical activation of cardiac afferent nerves.
Afferent neurons within cardiac sympathetic nerves can reflexly excite central sympathetic outflow. However, their contribution to cardiovascular control remains unclear because they are potentially opposed by inhibitory reflexes of cardiac vagal or arterial baroreceptor afferent origin. It was considered that sympathetically mediated, excitatory responses might be more prominent when initiated by chemical stimulation. In chloralose-anesthetized, vagotomized, sinoaortic-denervated cats, epicardial or intracoronary administration of bradykinin or potassium chloride evoked renal nerve excitation and pressor responses mediated by cardiac sympathetic afferent nerves. When upper thoracic sympathetic nerves were severed, and vagal afferent nerves remained intact, bradykinin and potassium chloride produced inhibition of renal nerve activity and depressor responses. When sympathetic and vagal components of cardiac innervation remained intact, these substances produced excitation, inhibition, or no change in sympathetic outflow. Excitation occurred as often as inhibition. A similar pattern was observed when arterial baroreceptor nerves remained intact. These data illustrate that cardiac sympathetic afferent neurons can have significant excitatory influences on the cardiovascular system in spite of opposition by inhibitory afferent groups.
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D001794:Blood Pressure; D001920:Bradykinin / Q000494:pharmacology; D002415:Cats; D006321:Heart / Q000294:innervation*; D006339:Heart Rate; D007668:Kidney / Q000294:innervation*; D011189:Potassium Chloride / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology*; D012018:Reflex / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*
D011189:Potassium Chloride; D001920:Bradykinin