Basal nitric oxide production curtails arteriolar vasoconstrictor
responses to angiotensin ii in rat kidney.
Ikenaga, Hideki, Rachel W. Fallet, and Pamela K. Carmines.
Department of Physiology and Biophysics, University of Nebraska
Medical Center, Omaha, Nebraska 68198-4575
APStracts 3:0058F, 1996.
Experiments were performed to test the hypothesis that renal
arteriolar vasoconstrictor responses to angiotensin II (ANG II) are
curtailed through a mechanism that involves stimulation of endogenous
nitric oxide (NO) synthesis. The in vitro blood-perfused
juxtamedullary nephron technique was exploited to monitor arteriolar
lumen diameter responses to exogenous ANG II before and during
treatment with the NO synthase inhibitor Nw-nitro-l-arginine (l-NNA).
Under control conditions, 1 nM ANG II reduced afferent and efferent
arteriolar diameters by 13 and 11%, respectively. In the presence of
l-NNA, 1 nM ANG II decreased afferent diameter by 26% and efferent
diameter by 35%. This augmentation could not be attributed to the l
-NNA-induced decrease in baseline diameter. l-NNA also augmented
vasopressin responses, indicating a lack of agonist-specificity in
this interaction. ANG II reactivity during l-NNA treatment was not
enhanced when tissue NO activity was fixed at basal levels (exposure
to 1 [mu]M sodium nitroprusside). These results indicate that
endogenous NO modulates the vasoconstrictive impact of ANG II on both
afferent and efferent arterioles of juxtamedullary nephrons, and that
this process does not require stimulation of NO synthesis.
Received 19 January 1996; accepted in final form 12 March 1996.
APS Manuscript Number F22-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96