Adding converting-enzyme inhibitors to the salt depleted state is marked by a reduction in blood pressure despite compensatory increases in heart rate and plasma norepinephrine. This study investigated whether this increase in sympathetic function is also accompanied by an increase in beta-adrenergic receptor function. Ten subjects were studied following two separate five day hospitalizations on 10 mEq sodium diets while receiving either placebo or captopril. During low sodium with captopril, blood pressure and angiotensin II decreased, while heart rate, renin, norepinephrine and isoproterenol-stimulated cyclic AMP accumulation in lymphocytes increased. The results indicate that enhanced beta-adrenergic receptor function does accompany sympathetic activation during sodium restriction and converting enzyme inhibition and further support studies showing that the renin-angiotensin system plays the dominant role in blood pressure regulation in the sodium depleted state.