Actions of endogenous endothelin on glomerular hemodynamics in the
rat.
Qiu, Changbin, Lennie Samsell, and Chris Baylis.
Department of Physiology, Robert C. Byrd Health Sciences Center of
West Virginia University, P.O. Box 9229, Morgantown, WV 26506-9229,
Telephone: (304) 293-4991, FAX: (304) 293-3850
APStracts 2:0145R, 1995.
Both endothelin ETA/ETB receptors are distributed in the glomerular
microcirculation but their physiologic functions, if any, are
unknown. We used a nonpeptide mixed ETA/ETB receptor antagonist
(Bosentan) and a selective ETA receptor antagonist (BQ-123) to
investigate the glomerular hemodynamic actions of endogenous ET in
the anesthetized euvolemic rat. Blockade of ETA and ETB receptors
with Bosentan produced a small fall in systemic blood pressure and a
large fall in glomerular blood pressure due to a significant increase
in preglomerular (afferent) arteriolar resistance. Single nephron
glomerular filtration rate was not reduced because of an offsetting
rise in glomerular capillary ultrafiltration coefficient. Blockade of
the selective ETA receptor with BQ-123 had no effect on blood
pressure or glomerular hemodynamics. These observations indicate that
endogenous endothelin is of physiologic importance in control of
glomerular hemodynamics. Surprisingly, endogenous endothelin
tonically dilates, rather than contracts the preglomerular arteriole
and it also tonically lowers the glomerular capillary ultrafiltration
coefficient, probably by contracting the mesangial cell. All
physiologic glomerular actions of endothelin are mediated via the ETB
receptor.
Received 2 February 1995; accepted in final form 18 May 1995.
APS Manuscript Number R88-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.