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首页> 外文期刊>American Journal of Physiology >cGMP-mediated Ca2+ release from IP3-insensitive Ca2+ stores in smooth muscle (see comments)
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cGMP-mediated Ca2+ release from IP3-insensitive Ca2+ stores in smooth muscle (see comments)

机译：cGMP介导的Ca2 +从平滑肌中IP3不敏感的Ca2 +存储中释放（请参阅评论）

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Recent studies on the role of nitric oxide (NO) in gastrointestinal smooth muscle have raised the possibility that NO-stimulated cGMP could, in the absence of cGMP-dependent protein kinase (PKG) activity, act as a Ca(2+)-mobilizing messenger [K. S. Murthy, K.-M. Zhang, J.-G. f1p4 J. T. Grider, and G. M. Makhlouf. Am. J. Physiol. 265 (Gastrointest. Liver Physiol. 28): G660-G671, 1993]. This notion was examined in dispersed gastric smooth muscle cells with 8-bromo-cGMP (8-BrcGMP) and with NO and vasoactive intestinal peptide (VIP), which stimulate endogenous cGMP. In muscle cells treated with cAMP-dependent protein kinase (PKA) and PKG inhibitors (H-89 and KT-5823), 8-BrcGMP (10 microM), NO (1 microM), and VIP (1 microM) stimulated 45Ca2+ release (21 +/- 3 to 30 +/- 1% decrease in 45Ca2+ cell content); Ca2+ release stimulated by 8-BrcGMP was concentration dependent with an EC50 of 0.4 +/- 0.1 microM and a threshold of 10 nM. 8-BrcGMP and NO increased cytosolic free Ca2+ concentration ([Ca2+]i) and induced contraction; both responses were abolished after Ca2+ stores were depleted with thapsigargin. With VIP, which normally increases [Ca2+]i by stimulating Ca2+ influx, treatment with PKA and PKG inhibitors caused a further increase in [Ca2+]i that reverted to control levels in cells pretreated with thapsigargin. Neither Ca2+ release nor contraction induced by cGMP and NO in permeabilized muscle cells was affected by heparin or ruthenium red. Ca2+ release induced by maximally effective concentrations of cGMP and inositol 1,4,5-trisphosphate (IP3) was additive, independent of which agent was applied first. We conclude that, in the absence of PKA and PKG activity, cGMP stimulates Ca2+ release from an IP3-insensitive store and that its effect is additive to that of IP3.
机译：一氧化氮（NO）在胃肠道平滑肌中的作用的最新研究提出了NO刺激的cGMP可以在没有cGMP依赖性蛋白激酶（PKG）活性的情况下充当Ca（2+）动员的可能性信使[K. S.Murthy，K.-M.张建国f1p4 J. T. Grider和G. M. Makhlouf。上午。 J.生理学。 265（胃肠道。肝脏生理学.28）：G660-G671，1993]。在分散的胃平滑肌细胞中使用8-溴-cGMP（8-BrcGMP）以及NO和刺激内源性cGMP的血管活性肠肽（VIP）对这一概念进行了研究。在使用cAMP依赖性蛋白激酶（PKA）和PKG抑制剂（H-89和KT-5823）处理的肌肉细胞中，8-BrcGMP（10 microM），NO（1 microM）和VIP（1 microM）刺激了45Ca2 +的释放（ 45Ca2 +细胞含量降低21 +/- 3至30 +/- 1％）; 8-BrcGMP刺激的Ca2 +释放具有浓度依赖性，EC50为0.4 +/- 0.1 microM，阈值为10 nM。 8-BrcGMP和NO增加了胞浆游离Ca2 +浓度（[Ca2 +] i）并引起收缩; Ca2 +储存耗尽了毒胡萝卜素后，两种反应均被取消。对于VIP，通常通过刺激Ca2 +流入而增加[Ca2 +] i，用PKA和PKG抑制剂治疗会导致[Ca2 +] i进一步增加，并恢复为毒胡萝卜素预处理细胞中的对照水平。肝素或钌红既不影响透化的肌肉细胞中cGMP和NO引起的Ca2 +释放也不引起收缩。由最大有效浓度的cGMP和肌醇1,4,5-三磷酸（IP3）诱导的Ca2 +释放是累加的，与首先使用哪种药剂无关。我们得出的结论是，在没有PKA和PKG活性的情况下，cGMP刺激了IP3不敏感存储中Ca2 +的释放，其作用是IP3的作用的累加。

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