文献类型：期刊文章

作　　者：禹永春[1] 郭慧淑[1] 李英[1] 朴琳[1] 李林[1] 李在琉[1] 许文燮[1]

机构地区：[1]延边大学医学院消化生理研究室

出　　处：《Acta Pharmacologica Sinica》

基　　金：Project supported by the National Natural Science Foundation of China, № 3966026.

年　　份：2003

卷　　号：24

期　　号：8

起止页码：93-99

语　　种：中文

收录情况：AJ、BDHX、BDHX2000、BIOSISPREVIEWS、CAB、CAS、CSA、CSA-PROQEUST、CSCD、CSCD2011_2012、EBSCO、EMBASE、FSTA、IC、JST、PROQUEST、PUBMED、SCI-EXPANDED(收录号：WOS:000184722600014)、SCIE、SCOPUS、WOS、ZGKJHX、核心刊

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 （InsP₃R）. However, ryanodine 10 μmol/L, an inhibitor of calciuminduced calcium release （CICR）, did not inhibit the effect of SNP-induced increase of STOC. Methylene blue （1 μmol/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 IP₃-sensitive calcium pools, however, extracellular Ca²⁺ may not be involved in the process.

关 键 词：sodium nitroprusside  potassium channels  CALCIUM stomach  smooth muscle  pyloric antrum  NICARDIPINE HEPARIN RYANODINE patch-clamp techniques  

分 类 号：R9[药学类]