[Beta-receptor blockers: metabolic actions and therapeutic consequences (author's transl)].
Whereas the control of cardiac function occurs through the sympathetic nervous system via the beta 1-receptors, metabolic processes are controlled via beta 1- and/or beta 2-receptors accordingly. The inhibition occurring during the use of non-selective beta-receptor blockade of the beta 2-receptors also consequently leads undesirably to possible impairment of insulin secretion and especially to glycogenolysis in the skeletal musculature. The initially more intensely inhibited lipolysis under mixed beta-receptor blockade lead among other things to more severe changes in the lipoproteins than a predominantly beta 1-selective receptor blockade through reactive compensation procedures. Generally in the treatment of arterial hypertension, as also of cardiovascular disease with beta-receptor blocker, a beta 1-receptor blocker is preferred in order to avoid as far as possible disadvantageous metabolic actions of such treatment.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D001786:Blood Glucose / Q000378:metabolism; D004040:Dietary Carbohydrates / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy*; D007328:Insulin / Q000097:blood; D008053:Lipid Mobilization / Q000187:drug effects; D008055:Lipids / Q000097:blood
D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D004040:Dietary Carbohydrates; D007328:Insulin; D008055:Lipids
Beta-Rezeptoren-Blocker. Metabolische Wirkungen und Konsequenzen für die Therapie.