Beta-receptor blockade, physical activity, and metabolism.
The adaptation processes under physical activity are regulated through an increase in the sympathetic impulse, whereby the circulation adaptation is mediated specifically by way of beta1-receptors and the energy supply predominantly by way of beta2-receptors. The maximum performance capacity, therefore, is restricted through every form of beta-blockade. However, it follows from the receptor pattern that the mixed beta1/beta2-blockade exhibits a substantially clearer effect. For everyday performance, the predominant beta1-selective blockade represents practically no handicap. The special advantages of beta1-selective-compared to nonselective-blockade are discussed. Beta1-blockers practically do not affect glycogenolysis. Under beta1/beta2-blockers, hypoglycemia could reactively lead to reflective pressure increases and bradycardia through epinephrine release. Beta1-blockers additionally influence the cellular potassium homeostasis to a substantially lower extent. Under nonselective blockers, a distinct increase in the serum potassium and a retardation of the reuptake in the cells are observed. Also, lipolysis is strongly negatively influenced under nonselective blockers. Especially for atherogenesis, the important high-density lipoprotein cholesterol is negatively influenced under nonselective blockers in contrast to selective ones. Under these aspects, results are demonstrated that were obtained in 16 hypertensive patients treated with bisoprolol. In conclusion, beta1-selective blockers are largely "metabolically neutral" and are therefore to be preferred.
Lohmann
F W
FW
InnereAbteilung, Krankenhaus Neukölln, Berlin, FRG.
Loesment
W A
WA
Kaehler
H
H
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology* / Q000627:therapeutic use; D017298:Bisoprolol / Q000494:pharmacology* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism; D008066:Lipolysis / Q000187:drug effects / Q000502:physiology; D008074:Lipoproteins / Q000187:drug effects / Q000378:metabolism; D005082:Physical Exertion / Q000187:drug effects* / Q000502:physiology; D018342:Receptors, Adrenergic, beta-1 / Q000378:metabolism*; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism*
D000319:Adrenergic beta-Antagonists; D008074:Lipoproteins; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D005947:Glucose; D017298:Bisoprolol