AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 6 1516-R1521, Copyright © 1994 by American Physiological Society
Hormonal, renal, and metabolic alterations during hypertension induced by chronic inhibition of NO in rats
J. Navarro, A. Sanchez, J. Saiz, L. M. Ruilope, J. Garcia-Estan, J. C. Romero, S. Moncada and V. Lahera
Department of Physiology, Complutense University, Madrid, Spain.
The evolution of renal excretory function and circulating vasoactive
systems was studied during progressive increases in blood pressure (BP)
induced in rats by oral administration of NG-nitro-L-arginine methyl ester
(L-NAME; 5-30 mg/100 ml) for 5 wk. L-NAME induced a stepped elevation (P
< 0.05) in BP levels without changing creatinine clearance, urine flow,
or sodium excretion rate along the study. Reductions (P < 0.05) in
plasma renin activity and plasma aldosterone concentration were found only
during treatment with 30 mg/100 ml of L-NAME. Plasma norepinephrine and
epinephrine concentrations were elevated (P < 0.05) in the last week of
the study. Plasma concentrations of endothelin-1 and urinary excretion of
prostaglandin E2, 6-ketoprostaglandin F1 alpha, and thromboxane B2 were not
significantly affected by L-NAME. Similarly, no changes in plasma
concentrations of glucose, insulin, total cholesterol, or triglycerides
were observed. In summary, during long-term administration of L-NAME,
progressive increases in BP levels were observed without changes in either
sodium excretion or enhanced circulating vasoconstrictor activity. Thus, it
is likely that inhibition of synthesis of nitric oxide (NO) in the
vasculature leads to an imbalance between the tonic relaxing action of NO
and the influences of vasoconstrictor agents even when the latter remain at
normal levels.
