Insulin resistance in hypertension--a relationship with consequences?

Resistance to the action of insulin on glucose metabolism, with the ensuing compensatory hyperinsulinaemia, is closely linked to essential hypertension. The decreased insulin sensitivity observed in hypertensive patients is independent of obesity. Hyperinsulinaemia is likely to promote the dyslipidaemia that frequently accompanies the hypertensive state, and often presents as increased total and very low density lipoprotein (VLDL)-triglycerides, low high density lipoprotein (HDL)-cholesterol and, in some studies, elevated levels of low density lipoprotein (LDL)-cholesterol. Lipid abnormalities, hypertension and possibly hyperinsulinaemia act together to increase the risk of atherosclerotic disease manifestations in hypertensive patients. Acutely, insulin has been shown to stimulate sympathetic nervous system activity and transmembrane electrolyte transport, to promote sodium retention and to cause vascular wall changes, including increased cholesterol biosynthesis and smooth muscle proliferation. If these mechanisms operate on a chronic basis, the continuous exposure to elevated plasma insulin levels may play a pathogenetic role in the development of high blood pressure, and also of a predisposition toward atherosclerosis in patients with hypertension. Further studies are necessary to establish these hypothetical cause-effect relationship which, if shown to be true, will contribute to a more wide-ranging view of essential hypertension and the optimum strategy for antihypertensive treatment.