Many of the electrolyte derangements seen in chronic heart failure are related to activation of the renin-angiotensin system. Activation of the system may cause the retention of both sodium and water; the former is primarily related to the release of aldosterone and the latter is related to an angiotensin-mediated increase in thirst and decrease in the excretion of free water. The interaction of these mechanisms may explain why patients with chronic heart failure have higher values for total body sodium but lower values for serum sodium concentration than hypertensive patients or normal subjects. Activation of the renin-angiotensin system may also cause potassium depletion, which is manifest clinically by a decrease in both total body potassium and serum potassium concentration. These electrolyte disturbances may play a role in the development of ventricular arrhythmias. The renin-angiotensin system may also contribute to the development of magnesium deficits. These hormone-electrolyte interactions have important implications in the treatment of patients with heart failure, especially those in whom the renin-angiotensin system is pharmacologically inhibited.