Metabolic consequences of treating hypertension

Reduction of morbidity and mortality has been the aim of drug treatment for hypertension since its beginning in the 1950s. Its efficacy has been tested in many trials. An outstanding result of these trials has been their clear success in preventing stroke and stroke-related deaths and in decreasing the incidence of congestive heart failure (CHF) and renal disease. A similar success has not been achieved in reducing coronary heart disease endpoints. Diuretics and beta-blockers played a central role in these studies; however, their adverse effects on lipid metabolism have been cited as a possible explanation for the failure of antihypertensive therapy to affect coronary heart disease (CHD). Recently, the extent and significance of these lipid changes has been put into perspective, and new insights into the role of carbohydrate metabolism and insulin resistance in hypertension have emerged. The same drugs which adversely affect lipid metabolism also adversely affect carbohydrate metabolism, and more is becoming known about these mechanisms and their role in hypertension and its sequelae. Other classes of antihypertensive drugs such as the calcium antagonists, angiotensin converting enzyme (ACE) inhibitors, and alpha 1-antagonists do not share these adverse effects. It has become increasingly clear that effective antihypertensive therapy includes both the lowering of blood pressure and containment of the abnormalities that accompany the hypertensive state.