OBJECTIVES: 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. DESIGN: Antihypertensive doses of captopril, an angiotensin converting enzyme, and hydralazine, a non-specific vasodilator, were administered in sham-operated and two-kidney, two clip Goldblatt hypertensive rats subjected to various degrees of dietary sodium intake. METHODS: 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. RESULTS: 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 sodium-replete 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. CONCLUSION: 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.