Effects of β-blockers on glucose and lipid metabolism

• Published in: Current medical research and opinion 2010-03, Vol.26 (3), p.615-629
• Main Author: Fonseca, Vivian A.
• Format: Article
• Language: English
• Subjects: Adrenergic; Adrenergic beta-Antagonists - adverse effects; Adrenergic beta-Antagonists - therapeutic use; Beta-blockers; Blood Pressure - drug effects; Cardiac Output - drug effects; Cardiovascular Diseases - metabolism; Cardiovascular Diseases - prevention & control; Diabetes mellitus; Dyslipidemias; Glucose - metabolism; Humans; Hypertension; Lipid Metabolism - drug effects; Randomized Controlled Trials as Topic; Sympathetic Nervous System; Vascular Resistance - drug effects
• ISSN: 0300-7995; 1473-4877
• DOI: 10.1185/03007990903533681

Abstract Background: Activation of the sympathetic nervous system (SNS) has been linked to hypertension. Beta-blockers, which decrease SNS activation via β-adrenergic receptor antagonism, are effective in lowering blood pressure and reducing cardiovascular morbidity and mortality in several conditions, including post-myocardial infarction and heart failure. Despite these clinical benefits, many physicians are reluctant to prescribe β-blockers because of perceived negative metabolic effects, including reduced glycemic control, masking of hypoglycemia, insulin resistance, and dyslipidemia. Objective: This article reviews the pathophysiology of hypertension and either insulin resistance or dyslipidemia as well as treatment effects from glucose- and lipid-lowering regimens on cardiovascular morbidity and mortality. Based on a PubMed literature search from January 1980 to December 2008, the effects of nonvasodilating (atenolol, metoprolol, and propranolol) and vasodilating β-blockers (carvedilol, labetalol, and nebivolol) on parameters of glucose and lipid metabolism in hypertension are presented. Preference for clinical trial inclusion was given to randomized, controlled trials with at least 100 patients. Limitations of a drug class literature review may include trial inclusion bias with associated result skewing and underrepresentation of an individual agent, which may give different results. Results: Beta-blockers differ in terms of their mechanism of action and their effects on glucose and lipid metabolism. Nonvasodilating β-blockers reduce blood pressure in association with a cardiac output reduction and may increase or have no appreciable effect on peripheral vascular resistance. As a result, nonvasodilating β-blockers are associated with a worsening of glycemic and lipidic control. In contrast, vasodilating β-blockers reduce peripheral vascular resistance but have little or no effect on cardiac output. Numerous studies have established that vasodilating β-blockers are associated with more favorable effects on glucose and lipid profiles than nonvasodilating β-blockers. Conclusions: Improvements in glucose and lipid metabolism mediated by vasodilating β-blockers may help reduce coronary artery disease risk among high-risk patients with hypertension.