G-protein regulation of an L-type calcium channel current in canine jejunal circular smooth muscle.

Calcium entry into smooth muscle cells is essential to maintain contractility. In canine jejunal circular smooth muscle cells the predominant calcium entry pathway is through L-type calcium channels. The aim of this study was to determine the G-protein regulation of L-type calcium channel current (ICaL) in isolated canine jejunal circular smooth muscle cells. Barium (80 mM) was used as the charge carrier. GTP-gamma S and GTP increased maximal inward current from 118.7 +/- 12 pA to 227.5 +/- 21.5 pA (n = 8) and 174.6 +/- 10.1 pA (n = 6) respectively. The increase in inward current was blocked by nifedipine suggesting it was through L-type calcium channels. Pertussis toxin did not alter baseline ICaL while cholera toxin increased ICaL from 125 +/- 19 pA in controls (n = 6) to 347 +/- 30 pA (n = 4). Staurosporine inhibited the increase in current evoked by GTP-gamma S and calyculin further increased ICaL over the increase evoked by GTP-gamma S. The results suggest that cholera toxin sensitive G-proteins activate L-type calcium channels in isolated canine jejunal circular smooth muscle cells through protein phosphorylation.