Regulation of the beta-adrenoceptor-cAMP-system during dynamic exercise in patients with primary hypertension after acute beta-blockade.

Abstract

Beta-adrenoceptors on lymphocytes are acutely increased after dynamic exercise in normotensive subjects, but not in hypertensives. It was thus of interest to evaluate the acute regulation of the lymphocyte beta-adrenoceptor-adenylate-cyclase-cAMP-system (BAAS) in patients with primary hypertension during dynamic stress after acute beta-blockade. Density and affinity of beta 2-adrenoceptors, and intracellular cAMP concentrations (baseline and isoprenaline stimulated values) were measured on the peripheral mononuclear cells in 8 male patients with primary hypertension before and immediately after dynamic exercise on a bicycle (50-200 W) at baseline and after acute beta-blockade (2 h following 100 mg atenolol). Dynamic exercise causes no significant changes in receptor density and affinity, nor in basal cAMP values. After acute beta-blockade the dynamic stress-induced rise in mean arterial blood pressure was significantly (p < 0.01) reduced from 33 to 24 mmHg, and beta-adrenoceptor density significantly (p < 0.05) increased from 1320 to 2102 molecules/cell, whereas affinity remained unchanged. Baseline and stimulated cAMP concentrations increased significantly (p < 0.05) from 5.3 to 7.0 and from 2.1 to 3.5 pmol/10(6) cells, respectively. These findings suggest that in primary hypertension the regulation of the beta 2-adrenoceptor-adenylate-cyclase-cAMP-system is impaired on exercise and can be normalised by acute beta-blockade. Since atenolol predominantly blocks beta 1-adrenoceptors, the observed normalisation of the lymphocyte BAAS may reflect only an unspecific effect of antihypertensive therapy per se.