AJP - Endocrinology and Metabolism, Vol 272, Issue 1 E126-E132, Copyright © 1997 by American Physiological Society
Mechanisms of centrally administered ET-1-induced increases in systemic arterial pressure and AVP secretion
N. F. Rossi, D. S. O'Leary and H. Chen
Department of Medicine, Wayne State University School of Medicine, Detroit 48201, USA.
Endothelins (ET) within the central nervous system (CNS) alter systemic
cardiovascular responses and arginine vasopressin (AVP) secretion. These
experiments were designed to ascertain whether the rise in systemic
arterial pressure after central administration of ET-1 is mediated by
enhancing sympathetic outflow and/or circulating AVP. In Long-Evans (LE/LE)
rats, intracerebroventricular injection of 1-10 pmol ET-1 dose dependently
increased mean arterial pressure (MAP). Peak response occurred 7-12 min
after ET-1 and was inhibited by ETA receptor antagonism. Systemic
vasopressin (V1) receptor blockade did not inhibit the pressor response,
and rats with central diabetes insipidus (DI/DI) displayed an identical
rise in MAP. Ganglionic blockade prevented ET-1-induced hemodynamic
effects. Peak plasma AVP levels occurred 60 min after ET-1, as the pressor
response began to wane. In sinoaortic-denervated LE/LE rats, ET-1 elicited
a 10-fold increase in AVP secretion that coincided with the hemodynamic
changes and was blocked by BQ-123. Thus ET-1 via ETA receptors within the
CNS induced a concentration-dependent increase in systemic arterial
pressure mediated by enhanced sympathetic outflow but not by circulating
AVP. Reflex baroreceptor activation attenuated AVP release.
