The prolonged (3 months) effects of high sodium intake and sodium meclofenamate were studied in two groups of male spontaneously hypertensive rats. Group 1 (8 rats) received 1% NaCl in tap water ad libitum and served as control. Group 2 (8 rats) received, besides 1 % NaCl in tap water, 50 µg/ml of sodium meclofenamate per rat daily. Renal metabolic, hemodynamic and histologic studies were done at the end of the study. The renal functional studies were performed in the unanesthetized, unrestrained state. Group 2 rats developed significantly higher arterial pressures, renal vascular resistance and histologic changes (p < 0.005), larger left ventricular weights (p < 0.05) and significantly lower effective renal plasma flow, renal blood flow (p < 0.005) and glomerular filtration rate (p < 0.05) than group 1 rats. There were no differences between the two groups of rats with respect to heart rate, hematocrit, right ventricular weight, body weight, fluid intake, urine output, sodium and potassium excretion and serum electrolytes. The results suggest that the combination of high sodium intake and prostaglandin synthesis inhibition exert a greater damaging effect on the arterial pressure and renal function of spontaneously hypertensive rats than salt alone.