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首页> 外文期刊>Japanese Journal of Pharmacology >Palytoxin-Induced K+ Efflux from Heal Longitudinal Smooth Muscle of the Guinea-Pia
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Palytoxin-Induced K+ Efflux from Heal Longitudinal Smooth Muscle of the Guinea-Pia

机译:ly药诱导的豚鼠纵向平滑肌的K +外排

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References(27) Cited-By(3) In guinea-pig ileal longitudinal smooth muscle, both palytoxin (PTX) and carbachol (CCh) increased K+ efflux with an EC50 of 1.8×10-10 M and 4.1×10-7 M, respectively. Atropine (10-6 M) did not inhibit the K+ efflux due to PTX (3×10-9 M), but completely inhibited the efflux due to CCh (10-5 M). External Ca2+ removal and verapamil (10-5 M) did not change the PTX-induced K+ efflux, although the CCh-induced K+ efflux was inhibited about 77% and 71%, respectively. PTX-induced K+ efflux was reduced to 31% by a depletion of intracellular Ca2+. Tetraethylammonium (15 mM) inhibited the K+ efflux due to PTX or CCh to 61% or 75%, respectively. The PTX-induced K+ efflux was also inhibited by cymarin (3×10-8 M), ouabain (10-5 M) and digitoxin (10-5 M). These results suggest that the PTX-induced K+ efflux is less dependent on Ca2+ influx than that due to CCh. Furthermore, the binding sites for PTX in the ileal muscle of guinea-pig may be Na+, K+-ATPase, as has been suggested in other types of cells.
机译:参考文献(27)被引用(3)在豚鼠回肠纵向平滑肌中,palytoxin(PTX)和carbachol(CCh)均增加K +流出,EC50为1.8×10-10 M和4.1×10-7 M,分别。阿托品(10-6 M)不会抑制PTX(3×10-9 M)引起的K +流出,但完全抑制CCh(10-5 M)引起的流出。外部Ca2 +去除和维拉帕米(10-5 M)不会改变PTX诱导的K +外排,尽管CCh诱导的K +外排分别被抑制了约77%和71%。 PTX诱导的K +外排通过细胞内Ca2 +的消耗减少到31%。四乙铵(15 mM)抑制了PTX或CCh引起的K +外流至61%或75%。洋甘菊(3×10-8 M),哇巴因(10-5 M)和洋地黄毒苷(10-5 M)也抑制了PTX诱导的K +外流。这些结果表明,PTX诱导的K +流出比CCh引起的对Ca2 +流入的依赖性更小。此外,豚鼠回肠肌肉中PTX的结合位点可能是Na +,K + -ATPase,正如在其他类型的细胞中所暗示的那样。

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