title: Beta-blocking agents in patients with insulin resistance: effects of vasodilating beta-blockers.
abstract: Essential hypertension is--at least in many subjects--associated with a decrease in insulin sensitivity, while glycaemic control is (still) normal. It seems that in hypertensive patients, two major functions of insulin are impaired: there is insulin resistance of peripheral glucose uptake (primarily skeletal muscle) and insulin resistance of insulin-stimulated vasodilation. In view of some retrospective data and meta-analyses, which showed a less than expected reduction in coronary events (coronary paradox), the metabolic side effects of the antihypertensive treatment have received more attention. Many groups have shown that conventional antihypertensive treatment, both with beta-blockers and/or diuretics, decreases insulin sensitivity by various mechanisms. While low-dose diuretics seem to be free of these metabolic effects, there is no evidence for this in the beta-adrenergic blockers. However, recent metabolic studies evaluated the effects of vasodilating beta-blockers, such as dilevalol, carvedilol and celiprolol, on insulin sensitivity and the atherogenic risk factors. None of them decreased insulin sensitivity, as has been described for the beta-blockers with and without beta1 selectivity. This supports the idea that peripheral vascular resistance and peripheral blood flow play a central role in mediating the metabolic side effects of the beta-blocking agents, as the vasodilating action (either via beta2 stimulation or alpha1-blockade) seems to more than offset the detrimental effects of the blockade of beta (or beta1) receptors. Further studies are needed to elucidate the relevance of the radical scavenging properties of these agents and their connection to their metabolic effects. Therefore, the beneficial characteristics of these newer beta-adrenoreceptor blockers suggest that the vasodilating beta-blocking agents could be advantageous for hypertensive patients with insulin resistance or type 2 diabetes.
authors.affiliation: Department of Endocrinology and Metabolism, Eberhard-Karls-University, Tübingen, Germany. snjacob@med.uni-tuebingen.de
authors.forename: S
authors.initials: S
authors.lastname: Jacob
authors.forename: B
authors.initials: B
authors.lastname: Balletshofer
authors.forename: E J
authors.initials: EJ
authors.lastname: Henriksen
authors.forename: A
authors.initials: A
authors.lastname: Volk
authors.forename: B
authors.initials: B
authors.lastname: Mehnert
authors.forename: K
authors.initials: K
authors.lastname: Löblein
authors.forename: H U
authors.initials: HU
authors.lastname: Häring
authors.forename: K
authors.initials: K
authors.lastname: Rett
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D050260:Carbohydrate Metabolism; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050356:Lipid Metabolism; D018384:Oxidative Stress; D012307:Risk Factors; D014665:Vasodilator Agents / Q000627:therapeutic use*
chemical_list: D000319:Adrenergic beta-Antagonists; D007328:Insulin; D014665:Vasodilator Agents