Hypertension, Vol 21, 660-666, Copyright © 1993 by American Heart Association
DM Pollock, JS Polakowski, BJ Divish and TJ Opgenorth
Blockade of the renin-angiotensin system was studied in male Sprague-
Dawley rats during long-term inhibition of nitric oxide synthase. Nitro-
L-arginine-methyl ester (L-NAME) was placed in the drinking water for 4
weeks (approximately 100 mg/kg per day). Separate groups of rats were
coadministered the angiotensin II antagonist A-81988 in the drinking water
ranging from approximately 0.001 to 1 mg/kg per day. Control groups
received only tap water or A-81988 alone. Each week, rats were placed in
metabolic cages, and tail-cuff blood pressures and blood samples were
taken. L-NAME produced a sustained elevation in tail-cuff pressure that was
completely prevented by A-81988. No changes in creatinine clearance, sodium
excretion, plasma creatinine concentration, or blood urea nitrogen were
observed. Food and water intakes were identical in all groups. Water
excretion was significantly increased in L-NAME-treated animals regardless
of additional inhibitor treatment, suggesting a possible role for nitric
oxide synthase in the control of water excretion; this effect was
independent of blood pressure. Although less potent than A-81988, the
angiotensin II antagonist losartan and the angiotensin converting enzyme
inhibitor enalapril also blocked L-NAME-induced hypertension. In a separate
series of experiments, rats were not given A-81988 until 2 weeks after
hypertension had fully developed in L-NAME-treated rats. Within 1 week of
treatment with the angiotensin II antagonist, tail-cuff pressure returned
to normal. We conclude from these studies that long-term inhibition of
endogenous nitric oxide production produces an angiotensin II-dependent
form of hypertension.
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Angiotensin blockade reverses hypertension during long-term nitric oxide synthase inhibition
Abbott Laboratories, Abbott Park, IL 60064.
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