Metabolic changes in essential hypertension may complicate the primary disease, or drug and nondrug intervention, or both. These changes include disturbances in renal function, the metabolism of urate, glucose and lipids, and in cation transport across plasma membranes. Some of these disorders may be worsened by the chronic administration of antihypertensive drugs like diuretics, beta-adrenoceptor antagonists, and the angiotensin converting enzyme inhibitors. Recent randomised controlled trials of antihypertensive drugs showed that the apparently adequate control of hypertension with a thiazide or beta-antagonist does not consistently prevent cerebrovascular and cardiac deaths and morbidity, and that beta-antagonists protect only nonsmoking men against cardiac death. One explanation is that blood pressure may not have been lowered enough. By contrast, cardiac deaths may be increased in patients whose diastolic pressure is reduced below 85-90 mmHg. The adverse metabolic effects of antihypertensive drugs may in part offset their protective benefits. However, population evidence does not support the general avoidance of thiazides or beta-antagonists in mild hypertension. Where possible drug treatment should be tailored to individuals according to their general condition, age, and any concurrent disease or medication.