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首页> 外文期刊>Life sciences >Both endothelium and afferent nerve endings play a role in acetylcholine-induced renal vasodilation
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Both endothelium and afferent nerve endings play a role in acetylcholine-induced renal vasodilation

机译：内皮和传入神经末梢均在乙酰胆碱诱导的肾血管舒张中起作用

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摘要

We investigated the nature and signaling pathways of endothelium- and sensory-nerve ending-derived substances involved in acetylcholine-induced vasodilation in rat isolated perfused kidney. Endothelial denudation by Triton X-100 (0.2%, 0.1 ml) or depletion of afferent nerve endings by capsaicin (10(-6) mol/l) attenuated acetylcholine-induced vasodilation. When these two. agents were administered together, the response to acetylcholine was completely inhibited. CGRP1 receptor blocker CGRP 8-37 (10(-7) mol/l) and adenosine A(2) receptor antagonist ZM 241 385 (10(-7) mol/l) inhibited acetylcholine-induced dilation. When indomethacin (10(-5) mol/l), a cyclooxygenase inhibitor, L-NOARG (10(-4) mol/l), a nitric oxide (NO) synthase inhibitor, and potassium chloride (30 mmol/l), to test EDHF response, were perfused simultaneously, the inhibition was greater than that was observed with each agent alone. Guanylate cyclase inhibitor ODQ (10(-5) mol/l) or protein kinase A inhibitor KT 5720 (5 x 10(-7) mol/l) inhibited acetylcholine-induced dilation. Gap junction uncoupler 18 alpha-glycyrrhetinic acid (10(-4) mol/l) caused an uncontrollable increase in basal perfusion pressure making it impossible to test against acetylcholine-induced dilation. Our data suggest that NO, prostanoids, EDHF, and CGRP released from vascular endothelium and afferent nerve endings participate in acetylcholine-induced vasodilation and their signal transduction molecules include protein kinase A and guanylate cyclase. (c) 2006 Elsevier Inc. All rights reserved.
机译：我们调查了大鼠离体灌注肾脏中参与乙酰胆碱诱导的血管舒张的内皮和感觉神经末梢衍生物质的性质和信号通路。 Triton X-100（0.2％，0.1 ml）对内皮的剥脱作用或辣椒素（10（-6）mol / l）对传入神经末梢的清除作用减弱了乙酰胆碱诱导的血管舒张作用。当这两个。药物一起给药，对乙酰胆碱的反应被完全抑制。 CGRP1受体阻滞剂CGRP 8-37（10（-7）mol / l）和腺苷A（2）受体拮抗剂ZM 241385（10（-7）mol / l）抑制了乙酰胆碱诱导的扩张。当使用吲哚美辛（10（-5）mol / l），环氧合酶抑制剂，L-NOARG（10（-4）mol / l），一氧化氮（NO）合酶抑制剂和氯化钾（30 mmol / l）时，为了测试EDHF反应，同时灌注，其抑制作用大于单独使用每种药物所观察到的抑制作用。鸟苷酸环化酶抑制剂ODQ（10（-5）mol / l）或蛋白激酶A抑制剂KT 5720（5 x 10（-7）mol / l）抑制乙酰胆碱诱导的扩张。间隙连接解偶联剂18α-甘草次酸（10（-4）mol / l）导致基础灌注压力不可控制地增加，从而无法测试对乙酰胆碱诱导的扩张。我们的数据表明，从血管内皮和传入神经末梢释放的NO，前列腺素，EDHF和CGRP参与乙酰胆碱诱导的血管舒张，其信号转导分子包括蛋白激酶A和鸟苷酸环化酶。 （c）2006 Elsevier Inc.保留所有权利。

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