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Regulation of L‐type Ca2+ channels in rabbit portal vein by G protein αs and βγ subunits

1 The effect of purified G protein subunits αs and βγ on L‐type Ca2+ channels in vascular smooth muscle and the possible pathways involved were investigated using freshly isolated smooth muscle cells from rabbit portal vein and the whole‐cell patch clamp technique. 2 Cells dialysed with either Gαs or Gβγ exhibited significant increases in peak Ba2+ current (IBa) density (148 % and 131 %, respectively) compared with control cells. The combination of Gαs and Gβγ further increased peak IBa density (181 %). Inactive Gαs and Gβγ did not have any effect on Ca2+ channels. 3 The stimulatory effect of Gαs on peak IBa was entirely abolished by the protein kinase A inhibitor Rp‐8‐Br‐cAMPS, or the adenylyl cyclase inhibitor SQ 22536. On the other hand, the stimulatory response of Ca2+ channels to Gβγ was not affected by the protein kinase A inhibitors Rp‐8‐Br‐cAMPS and KT 5720, or by the Ca2+‐dependent protein kinase C inhibitor bisindolylmaleimide 1, but was completely blocked by the protein kinase C inhibitor calphostin C. Pretreatment of cells with phorbol 12‐myristate 13‐acetate for over 18 h prevented the stimulatory effect of Gβγ on peak IBa. In addition, acute application of phorbol 12,13‐dibutyrate enhanced peak IBa density in control cells, which could be entirely blocked by calphostin C. 4 These data indicate that enhancement of Ba2+ currents by Gαs and Gβγ can be attributed to increased activity of protein kinase A and protein kinase C, respectively. No direct membrane‐delimited pathway for Ca2+ channel regulation by activated Gs proteins could be detected in vascular smooth muscle cells.