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

AIM

To investigate the role of calcium mobilization in the calcium-activated potassium currents [IK(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 mol/L significantly increased IK(Ca), and enhanced the spontaneous transient outward currents (STOC). SNP-induced increase of IK(Ca) was not blocked by extracellular calcium-free solution (containing egtazic acid 10 micromol/L and nicardipine 5 micromol/L, an L-type calcium channel blocker. And SNP 100 micromol/L suppressed the L-type calcium currents (ICa). SNP-induced increase of STOC was inhibited by heparin 3 g/L, a potent inhibitor of inositol triphosphate receptor (InsP3R). However, ryanodine 10 micromol/L, an inhibitor of calcium-induced calcium release (CICR), did not inhibit the effect of SNP-induced increase of STOC. Methylene blue (1 micromol/L), an inhibitor of soluble guanylate cyclase, also inhibited such an effect.

CONCLUSION

The increase of IK(Ca) caused by SNP may be mediated by cGMP via IP3-sensitive calcium pools, however, extracellular Ca2+ may not be involved in the process.