Adverse metabolic effects have been associated with drugs used in the therapy of hypertension, especially diuretics and beta-blockers. These effects include electrolyte, glucose/insulin, lipid and uric acid disturbances. This may explain, at least in part, why early trials examining the impact of antihypertensive pharmacotherapy with diuretics and beta-blockers showed beneficial effects on coronary artery disease that fell disappointingly short of the predicted effect. Among therapeutic drugs, diuretics cause disturbances in electrolyte homeostasis, e.g. hypokalaemia, hypomagnesaemia, and hyponatraemia. In contrast, ACE inhibitors cause hyperkalaemia under certain circumstances. Both diuretics and beta-blockers, especially nonselective beta-blockers that lack intrinsic sympathomimetic capabilities, have been associated with disturbances in glucose/insulin metabolism and can cause deleterious alterations in the profile of circulating plasma lipids. Hyperuricaemia, associated with diuretic use, appears to be a problem only in those patients who are predisposed to high circulating levels of uric acid.