beta-adrenergic modulation of maxi-K channels in vascular smooth muscle via Gi through a membrane-delimited pathway.

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 beta-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 Gi protein was present in the pipette solution the stimulatory effect of isoproterenol disappeared. These results suggest that beta-adrenoceptor stimulation increases maxi-K channel activity via a membrane-delimited pathway, probably through pertussis toxin-sensitive G protein (Gi).