β-Adrenergic modulation of maxi-K channels in vascular smooth muscle via G_i through a membrane-delimited pathway

Abstract

 Direct modulation of large-conductance Ca²⁺-activated K⁺ (maxi-K) channel by receptor-associated G protein in rabbit mesenteric arterial smooth muscle cells was studied using the outside-out patch clamp technique. Applying a β-adrenoceptor agonist (isoproterenol) increased maxi-K channel activity by 75%, and the effect was almost completely abolished by pretreating the cells with pertussis toxin but not with cholera toxin. When the antibody against G_i protein was present in the pipette solution the stimulatory effect of isoproterenol disap-peared. These results suggest that β-adrenoceptor stimulation increases maxi-K channel activity via a membrane-delimited pathway, probably through pertussis toxin-sensitive G protein (G_i).