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To determine the possible relationship between the degree of dietary sodium intake and the development of renal failure during blockade of the renin-angiotensin system.Antihypertensive doses of captopril, an angiotensin converting enzyme, and hydralazine, a non-specific vasodilator, were administered in sham-operated and twokidney, two clip Goldblatt hypertensive rats subjected to various degrees of dietary sodium intake.The blood pressure, water intake, urine flow and sodium excretion of the animals were determined before and during a 3-day period of drug administration. Plasma concentrations of urea and creatinine were measured as indicators of renal function and glomerular filtration rate.The blood pressure of the clipped rats was higher than that of sham-operated rats (241 ± 5 versus 150 ± 4 mmHg), regardless of their sodium intake. Captopril administration failed to lower blood pressures of sodiumreplete hypertensive rats, but in hypertensive rats fed either a low- or a 'no'-sodium diet the blood pressure was reduced by 45 ± 7 and 127 ± 19 mmHg, respectively. Furthermore, hydralazine reduced blood pressure in hypertensive rats fed a 'no'-sodium diet by a similar degree, to 99 ± 8 mmHg. Captopril, but not hydralazine, significantly increased plasma levels of urea and creatinine in hypertensive rats fed the 'no'-sodium diet.These findings indicate that angiotensin II plays an important role in the maintenance of renal function during blood pressure reduction by angiotensin converting enzyme inhibition in volume-contracted renovascular hypertensive states.