Contribution of β1‐ and β2‐adrenoceptors of human atrium and ventricle to the effects of noradrenaline and adrenaline as assessed with (−)‐atenolol

Abstract
(−)‐Atenolol was used as a tool to assess the function of β1 and β2‐adrenoceptors in human heart. Right atrial and left ventricular preparations from patients undergoing open heart surgery were set up to contract isometrically. Membrane particles were prepared for β‐adrenoceptor labelling with [3 H]‐(−)‐bupranolol and adenylate cyclase assays. The positive inotropic effects of (−)‐noradrenaline were antagonized to a similar extent by (−)‐atenolol in atrial and ventricular preparations. (−)‐Atenolol consistently antagonized the effects of (−)‐adrenaline to a lesser extent than those of (−)‐noradrenaline in atrial preparations. In ventricular preparations (−)‐atenolol antagonized the effects of low concentrations of (−)‐adrenaline to a lesser extent than those of high concentrations. pKB values (M) of (−)‐atenolol, estimated with non‐linear analysis from the blockade of the positive inotropic effects of the catecholamines, were 7.4 for β1‐adrenoceptors and 6.0 for β2‐adrenoceptors. (−)−Atenolol inhibited the binding of [3 H]‐(−)‐bupranolol to ventricular β1‐adrenoceptors with a pKD (M) of 5.9 and to ventricular β2‐adrenoceptors with a pKD of 4.6. (−)‐Atenolol inhibited the catecholamine‐induced adenylate cyclase stimulation in the atrium and ventricle with pKB values of 5.8‐6.4 for β1 and pKB values of 4.7‐5.7 for β2‐adrenoceptors. The binding and cyclase assays suggest a partial affinity loss for (−)‐atenolol inherent to membrane preparations. β1 ‐Adrenoceptors mediate the maximum positive inotropic effects of (−)‐noradrenaline in both the atrium and ventricle of man. β2‐Adrenoceptors appear to be capable of mediating maximal positive inotropic effects of (−)‐adrenaline in atrium. In contrast, ventricular β2‐adrenoceptors mediate only submaximal effects of (−)‐adrenaline.

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