pp36 and Hypertension--Renovascular

The aim of the study was to evaluate the effect of chronic inhibition of endothelin-1 (ET-1) synthesis on renovascular hypertension development. Male Wistar rats were subjected to an operation, according to the "1 kidney, 1 clip" method and were given an endothelin-converting enzyme inhibitor PP36 per os with drinking water for 4 weeks. Serum urea rose by 21% in hypertensive rats and by 44% in PP36 treated hypertensive rats. PP36 treatment resulted in blood pressure rise both in the Sham group (compared to the initial blood pressure level) and in hypertensive rats (compared to hypertensive control group). Significant reduction of circulating ET-1 after chronic PP36 administration by 28% was obtained only in normotensive, but not hypertensive rats. Circulating ET-1 was not altered in hypertensive rats, but ET-1 excretion rate was significantly enhanced by 90%, which was abolished by PP36. We suggest that chronic reduction of ET-1 synthesis in the kidney might lead to water and salt retention.

Topics: Animals; Aspartic Acid Endopeptidases; Deoxyuridine; Endothelin-1; Endothelin-Converting Enzymes; Hypertension, Renovascular; Kidney; Male; Metalloendopeptidases; Microsurgery; Propanolamines; Rats; Rats, Wistar; Renin-Angiotensin System; Salts; Urea; Water