Lesions of epinephrine neurons in the rostral ventrolateral medulla abolish the vasodepressor components of baroreflex and cardiopulmonary reflex

Abstract

Epinephrine-containing neurons of the rostral ventrolateral medulla (RVL) (the Cl group of Hokfelt) in the rat are primarily unilaterally innervated by neurons in the nucleus tractus solitarius (NTS) and in turn project to autonomic spinal neurons. In this study, we investigated whether the Cl area of the RVL mediates the vasodepressor responses (VDR) induced by either electrical stimulation of the vagus nerve or carotid sinus stretch. In all experiments, Cl neurons were localized immunocytochemically with antibodies to phenylethanolamine N-methyltransferase (PNMT). Bilateral lesions of the Cl area decreased arterial pressure (AP) and heart rate (HR) to spinal cord transection levels and blocked the VDR induced by vagal stimulation and carotid sinus stretch. Combined lesions of the contralateral NTS and Cl area ipsilateral to the stimulated vagus nerve maintained AP and HR at normal levels, and totally blocked the VDR to vagal stimulation and carotid sinus stretch. Since projections from the vagus nerve to NTS are bilateral and those from NTS to Cl unilateral, the combined contralateral NTS/ipsilateral Cl lesions isolated and interrupted the ipsilateral NTS-C1 pathway and, therefore, blocked the baroreceptor reflex. The results are consistent with the hypothesis that neurons in the NTS synapsing in or projecting through the Cl area mediate the baro- and cardiopulmonary mechanoreceptor reflex. © 1983 American Heart Association, Inc.