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Nitric oxide activates Ca2+-activated K+ channels in cultured bovine adrenal chromaffin cells.

机译:一氧化氮激活培养的牛肾上腺嗜铬细胞中的Ca2 +激活的K +通道。

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摘要

The effects of sodium nitroprusside (SNP) on Ca2+-dependent K+ (KCa) channels in cultured bovine adrenal chromaffin cells were investigated using single channel recording patch-clamp techniques. KCa channels were activated by application of 100 microM SNP to the extracellular side of cell-attached patches. Methylene blue (300 microM), an inhibitor of soluble guanylate cyclase, or H-8 (1 microM), a protein kinase inhibitor with relative specificity for cGMP-dependent protein kinase, diminished but did not completely abolish the SNP-induced KCa channel activation. Diethylamine/NO complex (DEA/NO), an NO donor, also activated KCa channels in cell-attached patches. Furthermore, application of 100 microM SNP or 100 nM DEA/NO to the intracellular surface of excised inside-out patches also activated KCa channels in the bath solution which contained 1 microM Ca2+. These results indicate that SNP is capable of activating the KCa channel via cGMP-dependent and -independent mechanisms. These studies demonstrate that NO may serve as an important regulatory mechanism for catecholamine secretion in chromaffin cells via the activation of KCa channels.
机译:使用单通道记录膜片钳技术研究了硝普钠(SNP)对培养的牛肾上腺嗜铬细胞Ca2 +依赖性K +(KCa)通道的影响。通过将100 microM SNP应用于细胞附着斑块的细胞外侧,可激活KCa通道。亚甲基蓝(300 microM),一种可溶性鸟苷酸环化酶抑制剂,或H-8(1 microM),一种对cGMP依赖性蛋白激酶具有相对特异性的蛋白激酶抑制剂,其作用减弱但并未完全消除SNP诱导的KCa通道激活。 NO供体二乙胺/ NO络合物(DEA / NO)也激活了细胞贴片中的KCa通道。此外,将100 microM SNP或100 nM DEA / NO应用于已切除的由内而外的贴剂的细胞内表面也激活了含1 microM Ca2 +的浴液中的KCa通道。这些结果表明SNP能够通过依赖于cGMP和独立于cGMP的机制激活KCa通道。这些研究表明,NO可能通过激活KCa通道,成为嗜铬细胞中儿茶酚胺分泌的重要调控机制。

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