Hypertension, Vol 22, 812-818, Copyright © 1993 by American Heart Association
PY Chen and PW Sanders
Nitric oxide is a potent endogenous vasodilator that regulates arterial
tone. A family of nitric oxide synthases uses L-arginine and L-
homoarginine stereospecifically as substrates for nitric oxide production
in vivo. By preventing expression of inducible but not constitutive nitric
oxide synthases, glucocorticoids differentiate which enzyme in this family
is the predominant source of nitric oxide generation in a given situation.
We proposed that defective production of nitric oxide produces
salt-sensitive hypertension in the Dahl/Rapp rat. Plasma concentrations of
L-arginine, citrulline, and ornithine of salt-sensitive (SS/Jr) and
salt-resistant (SR/Jr) rats on 8% sodium chloride chow for 1 week did not
differ. However, intravenous infusion of L-arginine and L-homoarginine, but
not D-arginine, increased urinary excretion of nitrate, the degradation
product of nitric oxide, and simultaneously lowered blood pressure in
hypertensive SS/Jr rats. Oral L-arginine also prevented development of
hypertension and increased urinary excretion of cyclic GMP and nitrate in
these rats. Dexamethasone, in a dose that prevented hypotension from
parenteral injection of lipopolysaccharide, completely prevented the
increase in excretion of cyclic GMP and nitrate, and hypertension resulted
despite concomitant treatment with L-arginine. These studies supported an
important role of dexamethasone-suppressible nitric oxide synthesis in the
prevention of salt-sensitive hypertension in the Dahl/Rapp rat.
ARTICLES
Role of nitric oxide synthesis in salt-sensitive hypertension in Dahl/Rapp rats
Nephrology Research and Training Center, University of Alabama at Birmingham 35294-0007.
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