|| Checking for direct PDF access through Ovid
Numerous antihypertensive drugs have been reported to cause adverse metabolic effects such as glucose intolerance and abnormal lipid metabolism.There is a well defined relationship between diuretic treatment and impaired glucose tolerance and dyslipidaemia. These effects, which are seen with thiazide diuretics and loop diuretics but not with spironolactone, are independent of body weight but are strongly dose-related.βBlockers without intrinsic sympathomimetic activity have adverse effects on lipid metabolism, but P-blockers with intrinsic sympathomimetic activity do not. From the metabolic point of view, the latter type of p-blockers represent the ideal choice, but they are rarely used today. All types of P-blockers can cause an increase in fasting blood glucose and impaired glucose tolerance.Neither ACE inhibitors nor calcium antagonists show any negative effects on glucose and/or lipid metabolism. ACE inhibitors have even been shown to improve insulin sensitivity. ACE inhibitors and calcium channel blockers are metabolically neutral, and there is evidence that combining an ACE inhibitor or calcium antagonist with a diuretic can reduce the adverse effects of the latter.Some calcium antagonists show a dose-dependent anti-oxidative activity. Lacidipine has the greatest anti-oxidative activity of the commonly used calcium channel blockers. Among ACE inhibitors, only captopril has anti-oxidative activity.Both genetic and modifiable factors may contribute to the metabolic effects of antihypertensive drugs.