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外向钾离子电流的激活:血管活性肠肽在食管中的作用

Activation of outward K+ currents: effect of VIP in oesophagus.

作者信息

Jury J, Daniel E E

机构信息

McMaster University, Department of Biomedical Sciences, Hamilton, Ontario, Canada.

出版信息

Br J Pharmacol. 1999 May;127(2):553-61. doi: 10.1038/sj.bjp.0702579.

DOI:10.1038/sj.bjp.0702579
PMID:10385258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1566048/
Abstract
  1. Electrical field stimulations (EFS) of the opossum and canine lower oesophageal sphincters (OLOS and CLOS respectively) and opossum oesophageal body circular muscle (OOBCM) induce non-adrenergic, non-cholinergic (NANC) relaxations of any active tension and NO-mediated hyperpolarization. VIP relaxes the OLOS and CLOS and any tone in OOBCM without major electrophysiological effects. These relaxations are not blocked by NOS inhibitors. Using isolated smooth muscle cells, we tested whether VIP acted through myogenic NO production. 2. Outward currents were similar in OOBCM and OLOS and NO increased them regardless of pipette Ca2+(i), from 50-8000 nM. L-NAME or L-NOARG did not block outward currents in OLOS at 200 nM pipette Ca2+. 3. Outward currents in CLOS cells decreased at 200 nM pipette Ca2+ or less but NO donors still increased them. VIP had no effect on outward currents in cells from OOBCM, OLOS or CLOS under conditions of pipette Ca2+ at which NO donors increased outward K+ currents. 4. We conclude, VIP does not mimic electrophysiological effects of NO donors on isolated cells of OOBCM, OLOS or CLOS. VIP relaxes the OLOS and CLOS and inhibits contraction of OOBCM by a mechanism unrelated to release of myogenic NO or an increase in outward current. 5. Also, the different dependence of outward currents of OOBCM and OLOS on pipette Ca2+ from those of CLOS suggests that different K+ channels are involved and that myogenic NO production contributes to K+ channel activity in CLOS but not in OLOS or OOBCM.
摘要
  1. 对负鼠和犬的下食管括约肌(分别为OLOS和CLOS)以及负鼠食管体环行肌(OOBCM)进行电场刺激(EFS),可诱导产生非肾上腺素能、非胆碱能(NANC)舒张,消除任何主动张力,并介导一氧化氮(NO)引起的超极化。血管活性肠肽(VIP)可舒张OLOS和CLOS以及OOBCM中的任何张力,且无明显电生理效应。这些舒张作用不受一氧化氮合酶(NOS)抑制剂的阻断。我们使用分离的平滑肌细胞,测试了VIP是否通过肌源性一氧化氮生成发挥作用。2. OOBCM和OLOS中的外向电流相似,且无论移液管中钙离子浓度(i)从50 nM至8000 nM,NO均可使其增加。在移液管钙离子浓度为200 nM时,L - 硝基精氨酸甲酯(L - NAME)或L - 硝基精氨酸(L - NOARG)不会阻断OLOS中的外向电流。3. 在移液管钙离子浓度为200 nM或更低时,CLOS细胞中的外向电流会降低,但NO供体仍可使其增加。在移液管钙离子浓度条件下,当NO供体增加外向钾离子电流时,VIP对OOBCM、OLOS或CLOS细胞中的外向电流无影响。4. 我们得出结论,VIP不会模拟NO供体对OOBCM、OLOS或CLOS分离细胞的电生理效应。VIP通过与肌源性NO释放或外向电流增加无关的机制舒张OLOS和CLOS,并抑制OOBCM的收缩。5. 此外,OOBCM和OLOS的外向电流对移液管钙离子浓度的依赖性与CLOS不同,这表明涉及不同的钾离子通道,且肌源性NO生成有助于CLOS中的钾离子通道活性,但对OLOS或OOBCM则无此作用。

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本文引用的文献

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Interstitial cells of Cajal mediate enteric inhibitory neurotransmission in the lower esophageal and pyloric sphincters.Cajal间质细胞介导食管下括约肌和幽门括约肌的肠抑制性神经传递。
Gastroenterology. 1998 Aug;115(2):314-29. doi: 10.1016/s0016-5085(98)70198-2.
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Myogenic NOS in canine lower esophageal sphincter: enzyme activation, substrate recycling, and product actions.
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Myogenic nitric oxide synthase activity in canine lower oesophageal sphincter: morphological and functional evidence.犬下食管括约肌的肌源性一氧化氮合酶活性:形态学和功能证据。
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Colocalization of inhibitory mediators, NO, VIP and galanin, in canine enteric nerves.
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Endogenous nitric oxide in the control of esophageal motility in humans.内源性一氧化氮对人体食管运动的调控作用
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Interplay of VIP and nitric oxide in the regulation of neuromuscular function in the gut.血管活性肠肽与一氧化氮在肠道神经肌肉功能调节中的相互作用。
Ann N Y Acad Sci. 1996 Dec 26;805:355-62; discussion 362-3. doi: 10.1111/j.1749-6632.1996.tb17496.x.
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Development of c-Kit-positive cells and the onset of electrical rhythmicity in murine small intestine.小鼠小肠中c-Kit阳性细胞的发育及电节律的起始
Gastroenterology. 1997 Jan;112(1):144-55. doi: 10.1016/s0016-5085(97)70229-4.
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Interstitial cells of Cajal mediate inhibitory neurotransmission in the stomach.Cajal间质细胞介导胃中的抑制性神经传递。
Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):12008-13. doi: 10.1073/pnas.93.21.12008.
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