Abnormalities of glucose, insulin, and lipoprotein metabolism are common in patients with hypertension. This constellation of risk factors may be recognized at young ages and is at least in part heritable. The insulin resistance and the compensatory hyperinsulinemia could be primary events, and enhanced sympathetic activity and diminished adrenal medullary activity would be important links between the defect in insulin action and the development of hypertension and the associated metabolic abnormalities. But not all hypertensive patients have insulin resistance. It is possible that insulin resistance, and compensatory hyperinsulinemia have major roles in the regulation of blood pressure in susceptible subjects predisposed to hypertension by heredity or environmental factors. Considerable evidence, both in experimental animal models and in humans, points to hypertension as of critical importance in the pathogenesis of severe diabetic heart disease. In diabetic hypertensive cardiomyopathy, coronary artery disease as well as structural and functional abnormalities are more pronounced than would be expected from either process alone. The hypertension increases the risk of diabetic nephropathy in non-insulin-dependent diabetic patients. The microalbuminuria is a powerful predictor of mortality in these patients. It seems that angiotensin-converting-inhibitors have efficacy in postponing nephropathy in hypertensive non-insulin-dependent diabetic patients. In patients with hypertension and diabetes, additional clinical trials are required to identify those interventions that will most effectively reduce not only overall risk but also definitive cardiovascular disease endpoints.