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Tulane University School of Medicine, Department of Physiology, New Orleans, Louisiana 70112
Experiments were
performed in anesthetized male Sprague-Dawley rats to determine whether
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 µg · 100 g
1 · min1)
decreased CBF by 21 ± 4% and MBF by 49 ± 8% and
increased blood pressure from 118 ± 1 to 140 ± 2 mmHg. 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 mmHg, which was a greater absolute increase than in
normotensive controls. Basal renal blood flow (RBF), estimated from
p-aminohippurate clearance and hematocrit, was similar in both the control (6.0 ± 0.5 ml · min1 · g1)
and hypertensive (6.0 ± 0.6 ml · min1 · g1)
rats. However, NLA-induced reductions in RBF averaged 60 ± 5% in
the hypertensive rats, compared with 31 ± 9% observed in control rats. GFR in control (0.97 ± 0.03 ml · min1 · g1)
and hypertensive rats (0.78 ± 0.12 ml · min1 · g1)
decreased to a similar extent during the first 30-min 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 · min1 · g1).
Basal urinary sodium excretion (0.2 ± 0.08 µeq · min1 · g1),
fractional excretion of sodium (0.3 ± 0.13%), and urine flow (4.9 ± 0.39 µl · min1 · g1)
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.
laser-Doppler flowmetry; cortical renal blood flow; medullary renal
blood flow; N-nitro-L-arginine; osmotic minipump
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