Abstract
To investigate the role of renal prostaglandin E2 (PGE2) in renovascular hypertension, urinary PGE2 was measured in rabbits with hypertension produced by left renal artery constriction. In the acute phase of renovascular hypertension (1 week after the constriction), urinary excretions of PGE2 and sodium were significantly increased without correlations with changes in the systemic blood pressure (delta BP). In this phase, delta BP was directly proportional to plasma renin activity and plasma aldosterone concentration (p less than 0.001). In the intermediate phase (5 weeks), delta BP lost significant correlations with plasma renin activity and plasma aldosterone concentration and had a inverse correlation with urinary sodium excretion (p less than 0.01). In the maintenance phase (10 weeks), delta BP showed inverse correlations (p less than 0.01) with both PGE2 and sodium excretions, although their excretions decreased to normal levels. In the clipped kidney, only urinary PGE2 excretion in the acute phase was significantly elevated (p less than 0.02), and both sodium and PGE2 excretions were significantly decreased (p less than 0.01) in the maintenance phase. In the nonclipped kidney, urinary PGE2 and sodium excretions were elevated in the acute and intermediate phases, but decreased to the control levels in the maintenance phase. In this phase, delta BP showed inverse correlation (p less than 0.01) with both PGE2 and sodium excretions from the nonclipped kidney. The infusion of saralasin, an angiotensin II analogue, dose dependently reduced the blood pressure in the acute phase, but showed no effect in the intermediate and maintenance phases.(ABSTRACT TRUNCATED AT 250 WORDS)
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