Adrenal epinephrine secretion is not regulated by sympathoinhibitory neurons in the caudal ventrolateral medulla

By providing the principal inhibitory regulation of the discharge of sympat hetic premotor neurons in the rostral ventrolateral medulla (RVLM), neurons in the caudal ventrolateral medulla (CVLM) play a major role in regulating the level of sympathetic nerve activity (SNA) to cardiovascular targets. T o determine whether adrenal medullary secretion of epinephrine (EPI) is als o regulated by sympathoinhibitory inputs from the CVLM to the RVLM, we comp ared levels of plasma EPI obtained after disinhibition of RVLM neurons with levels obtained after inhibition of CVLM neurons, both of which result in sustained elevations in arterial blood pressure (AP), SNA, and heart rate ( HR). Plasma norepinephrine (NE) concentrations were significantly elevated following bilateral microinjection either of bicuculline (BIC) into the RVL M or of muscimol into the CVLM of urethane/chloralose-anesthetized, artific ially-ventilated rats. In sharp contrast, although plasma EPI concentration s were significantly elevated following disinhibition of neurons in the RVL M, they were unchanged by inhibition of neurons in the CVLM. These results demonstrate that the discharge of sympathetic premotor neurons in the RVLM regulating adrenal secretion of EPI is modulated by a tonic, GABA-ergic inh ibition that arises from a source that is different from the sympathoinhibi tory neurons in the CVLM that project to RVLM sympathetic premotor neurons controlling vasoconstrictor and cardiac targets. (C) 1999 Published by Else vier Science B.V. All rights reserved.