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首页> 外文期刊>Pharmacological research: The official journal of The Italian Pharmacological Society >Role of potassium channels in the nitric oxide-independent vasodilator response to acetylcholine.
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Role of potassium channels in the nitric oxide-independent vasodilator response to acetylcholine.

机译：钾通道在不依赖一氧化氮的血管舒张剂对乙酰胆碱反应中的作用。

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摘要

Stimulation of vascular endothelial muscarinic receptors by acetylcholine (ACh) leads to the formation of an endothelium-derived relaxing factor (EDRF), which is generally accepted to be nitric oxide (NO). Recent evidence, however, suggests that NO may be only one of several EDRFs mediating the vasodilator response to ACh. Since this NO-independent vasodilator response to ACh has been hypothesized to be dependent upon K(+) channel activation, the current study was undertaken to investigate the role of K(+) channels in mediating the hindlimb vasodilator responses to ACh in vivo. Additionally, since variations in vascular tone can complicate the analysis of responses, the level of vascular tone was maintained at a similar level throughout the study so that responses could be compared directly. The results of the present study demonstrate that the vasodilator response to ACh possesses a significant component that is independent of NO production. The K(Ca) channel blockers charybdotoxin and apamin, but notK(+)-ATP channel blocker U37883A or the COX antagonist meclofenamate, attenuated the NO-independent component of the vasodilator response to ACh. This suggests that K(Ca) channels, but not K(+)-ATP channels or COX products, are involved in mediating the L-NAME resistant response to ACh. Further, the inhibition of the ACh vasodilator response by the K(+)-ATP opener BRL55834 suggests that the response is dependent upon membrane hyperpolarization. These data suggest that the mechanism mediating ACh responses in the hindlimb vascular bed of the rat are complex and may involve several signaling pathways.
机译：乙酰胆碱（ACh）对血管内皮毒蕈碱受体的刺激导致形成内皮源性舒张因子（EDRF），该因子通常被认为是一氧化氮（NO）。但是，最近的证据表明，NO可能只是介导ACh血管舒张反应的几种EDRF之一。由于已经假设这种对ACh的NO依赖性血管舒张反应依赖于K（+）通道激活，因此目前的研究旨在研究K（+）通道在介导体内对ACh的后肢血管舒张反应中的作用。另外，由于血管紧张度的变化会使反应分析复杂化，因此在整个研究过程中，血管紧张度水平保持在相似的水平，因此可以直接比较反应。本研究的结果表明，对ACh的血管舒张反应具有独立于NO产生的重要成分。 K（Ca）通道阻滞剂charybdotoxin和apapamin，而不是K（+）-ATP通道阻滞剂U37883A或COX拮抗剂甲氧芬酸，减弱了血管舒张剂对ACh的NO依赖性成分。这表明K（Ca）通道，但不参与K（+）-ATP通道或COX产物，不参与介导对ACh的L-NAME抗性反应。此外，K（+）-ATP开环剂BRL55834对ACh血管舒张反应的抑制作用表明该反应取决于膜超极化。这些数据表明介导大鼠后肢血管床中ACh反应的机制很复杂，可能涉及多种信号通路。

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