Abstract

Conflicting evidence exists regarding the ability of PGE 1 to normalize blood pressure in renal hypertensive rats. We performed experiments to determine the effect of PGE 1 (15 μg/kg i.p. daily for 3 weeks) in renal hypertensive Wistars and found no significant change in systolic pressure. A higher dose (150 μg/kg i.p.) lowered pressure after 14 days of treatment, but not back to control levels. Further investigations are required to establish the mechanism whereby PGE 1 evokes this fall. To test the hypothesis that endogenous prostaglandins have a hypotensive function in renal hypertension, experiments were performed using sodium meclofenamate to inhibit prostaglandin biosynthesis. In chronic hypertensive rats the drug had no significant effect, while in the acute phase of renal hypertension there was a dose-dependent inhibition of the pressure rise. The possibility is suggesteed that prostaglandins may initiate or sustain the acute phase of renal hypertension in rats.

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