Renin release from the kidneys is controlled by four major mechanisms - renal baroreceptors, the macula densa, the sympathetic nervous system and other humoral and ionic influences. Recently, the importance of the sympathetic nervous system in modulating renin release for a variety of stimuli has become apparent. The sympathetic adrenergic nerves act on a specific beta-receptor to stimulate renin release from the kidney. Those antihypertensive drugs that inhibit adrenergic nerve transmission tend therefore to lower plasma renin. beta-Adrenoreceptor blocking drugs also generally lower plasma renin by specific inhibition of renal renin release both in animals and humans. Diuretics and vasodilators in contrast elevate plasma renin levels. Plasma renin levels in hypertensive patients are the net result of many diverse influences, and similarly in patients treated with antihypertensive drugs the plasma renin level often is the result of opposing influences. Plasma renin levels tend to return towards normal levels after treatment in hypertensive patients. Plasma renin levels may offer a guide to a more rational basis for antihypertensive therapy in the future. However, the primary aim in treatment of the hypertensive patient should be to lower his blood pressure, independent of the effect of plasma renin levels.