Hypertension, Vol 23, 619-625, Copyright © 1994 by American Heart Association
RD Manning Jr and L Hu
The goal of this study was to determine whether nitric oxide has a long-
term role in the control of renal hemodynamics and the relation between
arterial pressure and urinary sodium excretion. Studies were conducted over
a 25-day period in seven conscious dogs equipped with indwelling vascular
catheters and an electromagnetic flow probe on the iliac artery. Nitric
oxide synthesis was inhibited by continuous intravenous infusion of
NG-nitro-L-arginine methyl ester at 37.1 nmol/kg per minute, and the
effects of low, normal, and high sodium intakes were determined.
Significant nitric oxide synthesis inhibition was evidenced by a decrease
in the depressor and flow responses to systemic acetylcholine
administration. During the normal sodium intake plus nitro-arginine period,
arterial pressure increased to hypertensive levels, averaging 120 +/- 4% of
control; renal vascular resistance increased to an average of 134 +/- 8% of
control; glomerular filtration rate and renal plasma flow decreased to 83
+/- 3% and 81 +/- 3% of control, respectively; and no changes occurred in
filtration fraction, plasma renin activity, plasma concentrations of
aldosterone and cortisol, urinary sodium excretion, sodium balance,
fractional excretion of sodium, urine volume, and volume balance. Arterial
pressure increased further to 130 +/- 3% of control during high salt
intake, and sodium balance was achieved at each sodium intake despite the
increase in arterial pressure because of a hypertensive shift in the
relation between urinary sodium excretion and arterial pressure.(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
Nitric oxide regulates renal hemodynamics and urinary sodium excretion in dogs
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
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