Hypokalemia modulates alpha- and beta-adrenoceptor bindings in rat skeletal muscle

Changes in the population of adrenergic alpha- and beta-receptors were examined in rat soleus muscles during hypokalemia by their direct determination using radiolabeled ligands. Only beta-adrenoceptors were detected in the normal rat muscles. Hypokalemia led to a pronounced decrease in beta-adrenoceptors, the number of [3H]DHA binding sites, by 50%, as compared with that in the normal rats. There was a genesis of alpha 1-adrenoceptors in hypokalemic rat muscles, since the competitive potency of adrenergic drugs against [3H]prazosin binding was in the order prazosin much greater than phentolamine greater than (+/-)-noradrenaline greater than yohimbine much greater than (+/-)-isoproterenol. The reduction of [3H]DHA binding sites was accompanied by an increase of an approximately equal amount in high-affinity [3H]prazosin binding sites. The Kd determined by kinetic analysis of [3H]prazosin binding was calculated from the ratio K-1/K1 that gave a value of 3.05 nM, which generally agreed with the 1.83 nM determined by saturation experiments (Scatchard plot). This phenomenon of a reduction in the beta-adrenoceptors and the occurrence of alpha 1-adrenoceptors in muscles during hypokalemia is discussed. alpha- and beta-adrenoceptors on soleus muscle membrane may play important but opposite roles in modulating potassium release from the muscle cells.