Role of nitric oxide in the arterial pressure and renal adaptations
to long-term changes in sodium intake.
Manning, R. Davis, Jr., Lufei Hu, and Jane F. Reckelhoff.
Department of Physiology and Biophysics, The University of
Mississippi Medical Center, 2500 North State Street, Jackson,
Mississippi 39216-4505
APStracts 3:0428R, 1996.
The goals of this study were to determine whether long-term nitric
oxide (NO) synthesis inhibition in dogs results in an increase in the
sodium-sensitivity of arterial pressure and whether changes in plasma
renin activity or the plasma concentrations of arginine vasopressin
(AVP) and aldosterone play an important role in this hypertension.
Studies were conducted in a control group and groups that received NO
inhibition with NG nitro-L-arginine methyl ester (L-NAME) at 10 or 25
[mu]g/kg/min. Each group was challenged with normal, low, and high
sodium intake for periods of five days each. Urinary nitrate +
nitrite excretion, UNOx, more than doubled in the control group
during high sodium intake. In both L-NAME groups, UNOx decreased
significantly, there was a hypertensive shift in the relation between
urinary sodium excretion and arterial pressure, and urinary sodium
excretion remained normal even in the high sodium intake period. L
-NAME infusion did not change the sodium sensitivity of arterial
pressure nor plasma renin activity, plasma aldosterone and plasma
AVP. In conclusion, the data suggest that in dogs increases in NO
synthesis are not necessary to excrete a chronic sodium load, and
decreases in NO do not increase the sodium sensitivity of arterial
pressure.
Received 17 July 1996; accepted in final form 20 November 1996.
APS Manuscript Number R409-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996