Beta-2 adrenergic blockade evaluated with epinephrine after placebo, atenolol, and nadolol

Abstract

Vascular (32-adrenergic blocking effects of the water-soluble drugs atenolol (β1-selective) and nadolol (nonselective) were evaluated. Twenty-four healthy young men were studied in three dosing groups (eight subjects per group) before and after 1 wk on placebo, atenolol (50 mg twice a day), or nadolol (40 mg twice a day). Maximal treadmill exercise heart rates were reduced to a similar degree by atenolol (-48 ± 3 bpm) and nadolol (-48 ± 4 bpm) but were not affected by placebo. Trough blood levels were 226 ± 9 ng/ml for atenolol and 43 ± 9 ng/ml for nadolol. Calf blood flow was measured with a plethysmograph and calf vascular resistance was calculated from blood pressure and flow. β2-Adrenergic blockade was determined at rest with epinephrine infused intravenously in graded doses from 0.001 to 0.032 μg/kg/ min. Mean arterial pressure and calf vascular resistance rose markedly after nadolol but not after atenolol or placebo. Marked bradycardia developed after nadolol, probably by baroreceptor stimulation. Thus at an equivalent, substantial degree of β1-adrenergic blockade, nadolol blocks vascular β2-adrenergic receptors and atenolol does not. Measurement of the peripheral vascular response to epinephrine infusion is an effective means of assessing the impact of β2-adrenergic blockers on vascular β2-adrenergic receptors. © 1985.