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Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48823
We showed
recently that endothelin (ET)A receptors are involved in
the salt sensitivity of ANG II-induced hypertension. The objective of
this current study was to characterize the role of endothelin
ETB receptor activation in the same model. Male rats on
fixed normal (2 meq/day) or high (6 meq/day) salt intake received a
continuous intravenous infusion of ANG II or salt only for 15 days.
During the middle 5 days of the infusion period, rats were given either
the selective ETB receptor antagonist A-192621 or the
nonselective endothelin receptor antagonist A-182086 (both at 24 mg · kg
1 · day1
intra-arterially). Infusion of ANG II caused a greater rise in arterial
pressure in rats on high-salt intake. The administration of A-192621
increased arterial pressure further in all rats. The chronic
hypertensive effect of A-192621 was not significantly affected by salt
intake or ANG II. The administration of A-182086 lowered arterial
pressure chronically only in rats on normal salt intake receiving ANG
II. Thus the salt sensitivity of ANG II-induced hypertension is not
caused by changes in ETB receptor function.
blood pressure; salt-sensitive hypertension; kidney
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