Role of calcium mobilization in sodium nitroprusside- induced increase of calcium-activated potassium currents in gastric antral circular myocytes of guinea pig

摘要

AIM: To investigate the role of calcium mobilization in the calcium-activated potassium currents [I_(K_(Ca)] increased by sodium nitroprusside (SNP), a nitric oxide (NO) donor, in gastric antral circular myocytes of the guinea pig. METHODS: A perforated patch-clamp technique was used, and the myocytes were isolated by collagenase. RESULTS: SNP 100 μmol/L significantly increased I_(K_(Ca)), and enhanced the spontaneous transient outward currents (STOC). SNP-induced increase of I_(K_(Ca)) was not blocked by extracellular calcium-free solution (containing egtazic acid 10 μmol/L and nicardipine 5 μmol/L, an L-type calcium channel blocker. And SNP 100 μmol/L suppressed the L-type calcium currents (I_(Ca)). SNP-induced increase of STOC was inhibited by heparin 3 g/L, a potent inhibitor of inositol triphosphate receptor (InsP_3R). However, ryanodine 10 μmol/L, an inhibitor of calcium-induced calcium release (CICR), did not inhibit the effect of SNP-induced increase of STOC. Methylene blue (1 mol/L), an inhibitor of soluble guanylate cyclase, also inhibited such an effect. CONCLUSION: The increase of I_(K_(Ca)) caused by SNP may be mediated by cGMP via IP_3-sensitive calcium pools, however, extracellular Ca~(2+) may not be involved in the process.