title: Hypokalemia modulates alpha- and beta-adrenoceptor bindings in rat skeletal muscle.
abstract: 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.
mesh_terms: D000818:Animals; D001667:Binding, Competitive; D007008:Hypokalemia / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D009132:Muscles / Q000032:analysis*; D011224:Prazosin / Q000378:metabolism; D011869:Radioligand Assay; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000032:analysis* / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000032:analysis*
chemical_list: D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D011224:Prazosin