The effects of chronic (8 days) intrarenal protaglandin E,(PGE,) infusion on arterial pressure and renal function were assessed using unilaterally nephrectomized dogs maintained on a fixed sodium intake of 55 mEq/day. During 5 days of continuous intrarenal PGE, infusion (2 Mg/min) alone, both urine output and water intake increased markedly, and urine osmolality fell. Despite nearly a 9-fold increase in both plasma aldosterone concentration and plasma renin activity, daily sodium excretion exceeded intake values an average of 10-15 mEq/day, and plasma sodium concentration tended to fall. Concomitantly, arterial pressure increased from 104±3 to 113±2 nun Hg (p< 0.05) on Day 5. Infusion of saralasin (40 min) transiently lowered pressure from 112±6 to 91±7 mm Hg. PGE, was infused in combination with SQ 14,225 for 3 additional days, resulting in a fall in arterial pressure to* steady-state value of 82±1 nun Hg. Concomitant with the fall in pressure, water and electrolyte excretion decreased during SQ 14,225+ PGE] infusion but, nonetheless, remained above control levels. In another group of dogs, continuous (6 days) intravenous infusion of prostaglandin F^,, at 25 Mg/min, had relatively moderate effects on water and electrolyte excretion and did not alter arterial pressure. Thus, it is unlikely that intrarenal conversion of PGE, to PGF2a, with subsequent release into the systemic circulation, contributed to the PGE,-induced pressure rise. We conclude that chronic intrarenal PGE, infusion results in mild hypertension, which is dependent upon the renin-angiotensin system, and is associated with polyuria, polydipsia, and moderate natriuresis.(Hypertension 2: 529-537, 1980)