Hypertension, Vol 17, 517-525, Copyright © 1991 by American Heart Association
L Lin, M Mistry, CT Stier Jr and A Nasjletti
We investigated the role of prostanoid-mediated pressor mechanisms in
setting the level of blood pressure in renin-dependent and renin-
independent models of hypertension in unanesthetized rats. Intravenous
administration of a blocker of thromboxane A2/prostaglandin endoperoxide
receptors, SQ29548 (2 mg/kg bolus injection plus 2 mg/kg/hr for 3 hours),
reduced from 162 +/- 4 to 144 +/- 5 mm Hg (p less than 0.05) the blood
pressure of rats with aortic coarctation- induced hypertension at 7-14 days
after coarctation when plasma renin activity is greatly increased. In
contrast, treatment with SQ29548 was without effect on the blood pressure
of either normotensive or hypertensive rats (i.e., aortic
coarctation-induced hypertension at 90- 113 days after coarctation,
deoxycorticosterone-salt-induced hypertension) having normal or depressed
values of plasma renin activity. The blood pressure-lowering effect of
SQ29548 in the early phase of aortic coarctation-induced hypertension was
positively correlated with the prevailing plasma renin activity and could
not be demonstrated in hypertensive rats pretreated with indomethacin. We
attribute the hypotensive effect of SQ29548 to interference with pressor
mechanisms that depend on activation of thromboxane A2/prostaglandin
endoperoxide receptors and suggest that such prostanoid-mediated mechanisms
are operational and contribute to an increase in blood pressure in
angiotensin-dependent forms of hypertension. Also prostanoid-mediated
vasodepressor mechanisms are operational in the early phase of aortic
coarctation-induced hypertension since the blood pressure of rats
pretreated with SQ29548 was increased by the subsequent administration of
indomethacin. Accordingly, the blood pressure of rats with aortic
coarctation-induced hypertension is influenced by the interplay of
prostanoid-mediated pressor and vasodepressor mechanisms.
ARTICLES
Role of prostanoids in renin-dependent and renin-independent hypertension
Department of Pharmacology, New York Medical College, Valhalla.
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