Glucose and insulin metabolism in hypertension.
Individuals with abnormal glucose and insulin metabolism have a higher incidence of hypertension, and recent interest has focused on the fact that patients with untreated essential hypertension have higher than normal plasma insulin concentrations, are resistant to insulin-stimulated glucose uptake and often have accompanying lipid disorders. The pathophysiological significance of these observations lies in the findings that insulin has mitogenic properties and can potentiate vascular smooth muscle growth, thus promoting structural changes in vessels and atherosclerosis. Insulin could also promote high blood pressure via its effect in increasing sodium reabsorption and sympathetic nervous system activity. A variety of therapies is available for treatment of hypertension in patients with metabolic complications. Lifestyle modification is considered to be the initial approach, with weight management the most important component. Although diuretics and beta-blockers have a proven record in reducing morbidity and mortality, they may have adverse effects on glucose, insulin and lipids and should be used with caution in hypertensive subjects with metabolic risks. alpha-adrenergic blockers have favorable effects on lipids and glucose. Calcium antagonists have no adverse effect on glucose or insulin in patients with essential hypertension or diabetic patients with hypertension. ACE inhibitors, on the other hand, have neutral or beneficial effects on glucose, insulin and lipid metabolism, improving insulin sensitivity, insulin secretion, potassium balance and intermediary metabolism. Finally, oral hypoglycemic agents, which improve glucose metabolism and insulin sensitivity, can reduce blood pressure in obese, hypertensive subjects.
Corry
D B
DB
Department of Medicine, UCLA San Fernando Valley Program, USA.
Tuck
M L
ML
D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D007328:Insulin / Q000378:metabolism* / Q000502:physiology; D007333:Insulin Resistance
D000959:Antihypertensive Agents; D001786:Blood Glucose; D007328:Insulin; D005947:Glucose