Renoprotective effects of nitric oxide in angiotensin ii-induced
hypertension in the rat.
Chin, So Yeon, Chi-Tarng Wang, Dewan S. A. Majid, and L. Gabriel
Navar.
Tulane University School of Medicine, Department of Physiology
SL39, 1430 Tulane Ave. New Orleans, LA. 70112, USA.
APStracts 5:0018F, 1998.
Experiments were performed in anesthetized male Sprague-Dawley rats to
determine if increased nitric oxide (NO) activity during the
development of hypertension exerts a protective effect on renal
cortical blood flow (CBF) and medullary blood flow (MBF). The effects
of acute NO synthase inhibition on renal function and on CBF and MBF,
measured by laser-Doppler flow probes, were evaluated in control and
Ang II-infused hypertensive rats, prepared by the infusion of Ang II
at a rate of 65 ng/min via osmotic minipumps implanted subcutaneously
for 13 days. In normotensive rats (N=8), intravenous infusion of N(
-nitro-L-arginine (NLA; 20 (g/100g(min) decreased CBF by 21 ( 4% and
MBF by 49 ( 8% and increased blood pressure from 118 ( 1 to 140 ( 2
mm Hg. In Ang II-infused rats (N=7), CBF and MBF decreased by 46 ( 5%
and 25 ( 6%, respectively during infusion of NLA. Arterial pressure
increased from 160 ( 5 to 197 ( 7 mm Hg which was a greater absolute
increase than in normotensive controls. Basal renal blood flow,
estimated from PAH clearance and hematocrit, was similar in both the
control (6.0 ( 0.5 ml/min(g) and hypertensive (6.0 ( 0.6 ml/min(g)
rats. However, NLA-induced reductions in RBF averaged 60 ( 5% in the
hypertensive rats, compared to 31 ( 9% observed in control rats. GFR
in control (0.97 ( 0.03 ml/min(g) and hypertensive rats (0.78 ( 0.12
ml/min(g) decreased to a similar extent during the first 30-minute
period of NLA infusion. GFR returned toward control levels in control
rats; in contrast, GFR remained significantly decreased in the Ang
II-infused rats (0.58 ( 0.11 ml/min(g). Basal urinary sodium
excretion (0.2 ( 0.08 (Eq/min(g), fractional excretion of sodium (0.3
( 0.13%) and urine flow (4.9 ( 0.39 (l/min(g) in hypertensive rats
did not increase significantly after NLA treatment as occurred in
normotensive controls. These data suggest that a compensatory
increase in nitric oxide activity partially counteracts the
vasoconstrictor influence of elevated Ang II levels to regulate renal
hemodynamics and maintain cortical perfusion in the renal
circulation.
Received 31 July 1997; accepted in final form 7 January 1998.
APS Manuscript Number F256-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 28 January 1998