[Arterial hypertension and disorders of hydrocarbon metabolism].
Abnormalities of glucose, insulin, and lipoprotein metabolism are common in patients with hypertension. This constellation of risk factors may be recognized at a young ages and is, at least in part, inheritable. Insulin resistance and compensatory hyperinsulinemia may be primary events, and enhanced sympathetic activity and diminished adrenal medullary activity could 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 hereditary or environmental factors. Considerable evidence, both in experimental animal models and in humans, points to hypertension as being 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. 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 the interventions that will most effectively reduce not only overall risk but also improve cardiovascular disease prognosis.
González Maqueda
I
I
Unidad Coronaria, Hospital La Paz, Madrid.
Roldán Rabadán
I
I
Armada Romero
E
E
Pereira Bouza
J
J
González Lama
I
I
D000419:Albuminuria / Q000150:complications; D000818:Animals; D003920:Diabetes Mellitus / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000209:etiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D006331:Heart Diseases / Q000209:etiology; D006801:Humans; D006946:Hyperinsulinism / Q000209:etiology*; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D007333:Insulin Resistance; D011379:Prognosis; D051381:Rats