Hypertension, Vol 19, 549-554, Copyright © 1992 by American Heart Association
LH Mortensen and GD Fink
The effect of salt intake on the hypertensive response to long-term
infusion of endothelin-1 was investigated. Chronically instrumented male
Sprague-Dawley rats (325-375 g) were used in a 15-day protocol that
included 3 control days followed by 7 days of endothelin-1 infusion at 5.0
pmol.kg-1.min-1 and 5 days of recovery. Rats were maintained on either a
normal sodium chloride intake (2.0 meq Na+ per day; normal sodium) or a
high sodium chloride intake (6.0 meq Na+ per day; high sodium) throughout
the protocol. Control rats received normal or high sodium intakes but not
endothelin-1. In high-sodium rats, endothelin-1 produced a significant
increase in mean arterial pressure and total peripheral resistance; a
significant bradycardia was observed only on the first day after the start
of the endothelin-1 infusion. Cardiac output, stroke volume, water balance,
and urinary sodium and potassium excretion remained unchanged. Termination
of endothelin-1 infusion resulted in rapid normalization of both arterial
pressure and peripheral resistance. In contrast, normal sodium rats
exhibited no alteration in mean arterial pressure, heart rate, total
peripheral resistance, stroke volume, water balance, or urinary sodium and
potassium excretion throughout the endothelin-1 infusion protocol. The
hypertension produced by endothelin-1 infusion cannot be explained by
alterations in salt or water balance since endothelin-1 infusion in high
sodium animals produced significant increases in mean arterial pressure
with no observable changes in water or electrolyte balance. These results
indicate that endothelin-induced hypertension in conscious rats is a
salt-dependent model of hypertension.
ARTICLES
Salt-dependency of endothelin-induced, chronic hypertension in conscious rats
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824.
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