Renal nerves contribute to the genesis of at least four disease processes. 1. Excess renal nerve activity contributes significantly to salt and water retention by patients with congestive circulatory failure. 2. Circumstantial evidence suggests that dopamine production may be deficient in a group of patients with idiopathic edema. Aldosterone secretion is high in this group and it has been shown that dopamine exerts a tonic inhibitory effect on angiotensin-stimulated aldosterone secretion. 3. Excess renal nerve activity probably plays a crucial role in the transition from hypotension and pre-renal failure to ischemic acute tubular necrosis. 4. Without doubt hyperactivity of renal nerves causes systemic hypertension in a variety of animal disease models. There is also good reason to believe that this ocurs in some forms of human hyptertension. The effects of the sympathetic nervous system on renal vascular resistance, renin release, tubular electrolyte reabsorption and aldosterone secretion are discussed in the context of these four diseases.