环amp依赖蛋白激酶不依赖血管紧张素ii诱导的鼠下颌下神经节神经元钙电流的抑制。

IF 0.5 Q4 DENTISTRY, ORAL SURGERY & MEDICINE

Bulletin of Tokyo Dental College Pub Date : 2002-05-01 DOI:10.2209/TDCPUBLICATION.43.95

T. Endoh, M. Abe, Takashi Suzuki

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引用次数: 0

摘要

在先前的研究中，我们证明血管紧张素II (AngII)抑制仓鼠下颌下神经节(SMG)神经元的电压依赖性钙通道(VDCCs)电流(ICa)。在窦房结细胞中，有报道称AngII通过抑制环AMP的产生来抑制ICa。在本研究中，为了探讨环AMP-环AMP依赖性蛋白激酶(PKA)途径在血管i诱导的ICa抑制中的可能参与，我们在SMG神经元中检测了PKA激活剂和抑制剂对AngII的影响。可透膜环AMP预处理神经元和PKA阻滞剂细胞内透析均不能减弱血管i诱导的ICa抑制。这些结果表明，在SMG神经元中，AngII通过一种不依赖amp - pka的循环机制抑制ICa。

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Cyclic AMP-dependent protein kinase-independent angiotensin II-induced inhibition of calcium current in hamster submandibular ganglion neurons.

In a previous study, we demonstrated that angiotensin II (AngII) inhibited voltage-dependent calcium channels (VDCCs) currents (ICa) in hamster submandibular ganglion (SMG) neurons. In sinoatrial node cells, it has been reported that AngII inhibits ICa by suppressing cyclic AMP production. In this study, to investigate the possible involvement of a cyclic AMP-cyclic AMP dependent protein kinase (PKA) pathway in the AngII-induced inhibition of ICa, effects of AngII were examined in SMG neurons after treatment with an activator and inhibitor of PKA. Neither pretreatment of neurons with membrane permeable cyclic AMP nor intracellular dialysis of PKA blocker attenuated the AngII-induced inhibition of ICa. These results indicate that AngII inhibited ICa via a cyclic AMP-PKA-independent mechanism in SMG neurons.

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来源期刊

Bulletin of Tokyo Dental College DENTISTRY, ORAL SURGERY & MEDICINE-

CiteScore

0.90

自引率

0.00%

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期刊介绍： The bulletin of Tokyo Dental collegue is principally for the publication of original contributions to multidisciplinary research in dentistry.