abstract
- The relationship between inositol-1,4,5-trisphosphate-sensitive Ca2+ stores and Ca2+ entry through potential-dependent L-type Ca2+ channels was examined using whole-cell voltage-clamp technique in cells of longitudinal muscle layer of guinea-pig ileum. It was found that heparin (10(-10) mol/l) in the pipette rapidly inhibited the current through L-type Ca2+ channels. Neither an inhibitor of the sarcoplasmic reticulum Ca2+ pump (cyclopiazonic acid) nor blockers of Ca(2+)-induced Ca2+ release (ryanodine or ruthenium red) affected the Ca2+ current. The failure of heparin to affect Ca(2+)-currents through L-type Ca2+ channels in cells from circular muscle of the same organ suggested that heparin had no direct effect on L-type Ca2+ channels. Thus the inhibition of the latter in heparin-loaded cells from the longitudinal layer is supposed to be Ca(2+)-dependent due to the overfilling of the inositol-1,4,5-trisphosphate-sensitive Ca2+ store.