Determinants of renal vasoconstriction after systemic inhibition of
nitric oxide synthesis in rats.
Brand-Schieber, E., M. Pucci, and A. Nasjletti.
Department of Pharmacology, New York Medical College, Valhalla, New
York
APStracts 3:0013R, 1996.
The effects of NG-nitro-L-arginine (L-NA, 10 mg/k, iv) on renal
hemodynamics were examined in control rats, rats in which renal
perfusion pressure was prevented from rising after L-NA by
constricting the abdominal aorta, and rats in which tubuloglomerular
feedback was inhibited by furosemide pretreatment, ureteral ligation,
or both interventions combined. In control rats, L-NA increased
(P<0.05) renal vascular resistance (274+27%) along with systemic
arterial (54+4%) and renal perfusion (54+5%) pressures, and decreased
(P<0.05) renal blood flow (57+4%). In rats in which renal
perfusion pressure was prevented from increasing along with systemic
arterial pressure (54+4%), the L-NA-induced elevation of renal
vascular resistance (173+27%) was less intense (P<0.05). In
another study, where renal perfusion pressure was fixed at pre-L-NA
levels, L-NA-induced increases in renal vascular resistance (130+20%)
were attenuated (P<0.05) further with furosemide pretreatment
(52+12%), with ureteral ligation (75+10%) and with furosemide
pretreatment and ureteral ligation combined (32+8%). These data
suggest that vasoconstrictor mechanisms linked to tubuloglomerular
feedback and perfusion pressure elevation contribute to renal
vasoconstriction after systemic inhibition of nitric oxide synthesis
with L-NA.
Received 9 August 1995; accepted in final form 13 December 1995.
APS Manuscript Number R503-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96