Results of attempts to correlate levels of pressor substance with increase in blood pressure (BP) in hypertension have at best been equivocal. However, much experimental evidence seems to indicate that failure of the renal antihypertensive system may play an important role in the development of experimental renal hypertension. Among the antihypertensive principles isolated from the kidney, only prostaglandins (PG) have been chemically characterized. Their pharmacological actions have been well defined but their physiological significance remains obscure. The purpose of the present proposal is to further elucidate the role that PG might play in renal hypertension and during its reversal. For this purpose, patterns of change in systemic blood pressure, urinary sodium excretion, plasma and renal concentrations of PG and renin will be studied: a) Before and after blockade of PH synthesis with indomethacin during the development and reversal of renal hypertension, and b) During intra-arterial and intervenous infusion of Pg to renal hypertensive animals. Special emphasis will be placed on assessing the role of the kidney in mediating the hypotensive response to PG infusion.