AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 3 568-R572, Copyright © 1993 by American Physiological Society
Endothelium-derived relaxing factor responses in Doca-salt hypertensive rats
K. A. Kirchner, P. H. Scanlon Jr, D. J. Dzielak and R. L. Hester
Department of Medicine, University of Mississippi Medical Center, Jackson 39216-4505.
This study examined the contribution of endothelium-derived relaxing factor
(EDRF) to the susceptibility of uninephrectomized rats to
deoxycorticosterone acetate (DOCA)-salt hypertension. N
omega-nitro-L-arginine, a probe for EDRF, produced smaller increases (P
< 0.001) in mean arterial pressures in anesthetized hypertensive
DOCA-salt rats than in sham rats. Acute L-arginine administration (300
mg/kg body wt i.v.) failed to reduce pressure in anesthetized DOCA-salt
rats. Chronic oral and intraperitoneal L-arginine did not lower pressure in
conscious DOCA-salt rats with established hypertension, nor did it prevent
hypertension when begun in prehypertensive DOCA-salt rats. Preconstricted
aortic rings from DOCA-salt rats had attenuated relaxation to acetylcholine
compared with sham rats. Rings L-arginine-treated DOCA-salt rats had
responses similar to DOCA-salt rats. Relaxation to nitroprusside was not
different between any rat group. Thus EDRF is attenuated in DOCA-salt
hypertension. However, unlike several other hypertensive models, the
blunted EDRF response cannot be overcome by provision of L-arginine. These
data suggest synthesis or release of EDRF may be noncompetitively inhibited
in DOCA-salt hypertension.
