Abstract

The present study was designed to investigate the properties of spontaneous transient inward currents generated by interstitial cells (ICs) in the rabbit portal vein. Single ICs were freshly isolated from smooth muscle of the rabbit portal vein enzymetically. Using whole-cell patch clamp techniques, the spontaneous transient inward currents (STICs) were recorded at −60 mV of holding potential in freshly dispersed ICs. Both gadolinium, a non-selective cation channel inhibitor, and niflumic acid, a calcium-activated chloride channel blocker, abolished the inward currents. Replacement of external Na + with N-methyl- d-glucamine (NMDG +) also blocked the inward currents. The inward currents were abolished by caffeine, carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP), thapsigargin and ryanodine, but were partly inhibited by 2-aminoethoxydiphenyl borate (2-APB). W-7, a calmodulin inhibitor, increased the amplitude of the inward currents. These results suggest that non-selective cation channels are involved in the generation of the spontaneous transient inward currents recorded from ICs. The currents are regulated by intracellular calcium and calmodulin. But in the present study, the involvement of the calcium-activated chloride channels in the generation of the currents cannot be excluded.

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