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首页> 外文期刊>American Journal of Physiology >Regulation of pulmonary venous tone in response to muscarinic receptor activation.
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Regulation of pulmonary venous tone in response to muscarinic receptor activation.

机译：响应毒蕈碱受体活化而调节肺静脉张力。

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We investigated cellular mechanisms that mediate or modulate the vascular response to muscarinic receptor activation (ACh) in pulmonary veins (PV). Isometric tension was measured in isolated canine PV rings with endothelium (E+) and without endothelium (E-). Tension and intracellular Ca(2+) concentration ([Ca(2+)](i)) were measured simultaneously in fura-2-loaded E- PV strips. In the absence of preconstriction, ACh (0.01-10 microM) caused dose-dependent contraction in E+ and E- rings. ACh contraction was potentiated by removing the endothelium or by nitric oxide (NO) synthase inhibition (N-nitro-L-arginine methyl ester, P = 0.001). Cyclooxygenase inhibition (indomethacin) reduced ACh contraction in both E+ and E- PV rings (P = 0.013 and P = 0.037, respectively). ACh contraction was attenuated by inhibitors of voltage-operated Ca(2+) channels (nifedipine, P < 0.001), inositol-1,4,5-trisphosphate (IP(3))-mediated Ca(2+) release (2-aminoethoxydiphenyl borate, P = 0.001), PKC (bisindolylmaleimide I, P = 0.001), Rho-kinase (Y-27632, P = 0.002), and tyrosine kinase (TK; tyrphostin 47, P = 0.015) in E- PV rings. ACh (1 microM) caused a leftward shift in the [Ca(2+)](i)-tension relationship (P 0.015), i.e., ACh increased myofilament Ca(2+) sensitivity. Inhibition of PKC, Rho-kinase, and TK attenuated the ACh-induced increase in myofilament Ca(2+) sensitivity (P < 0.001, P < 0.001, and P = 0.024, respectively). These findings indicate that in canine PV, ACh contraction is modulated by NO and partially mediated by metabolites of the cyclooxygenase pathway and involves Ca(2+) influx through voltage-operated Ca(2+) channels and IP(3)-mediated Ca(2+) release. In addition, ACh induces increased myofilament Ca(2+) sensitivity, which requires the PKC, Rho-kinase, and TK pathways.
机译：我们研究了介导或调节肺静脉（PV）中毒蕈碱受体激活（ACh）的血管反应的细胞机制。在带有内皮（E +）和不带有内皮（E-）的孤立犬PV环中测量了等轴测张力。张力和细胞内Ca（2+）浓度（[Ca（2 +）]（i））在呋喃2加载的E-PV试纸中同时测量。在没有预收缩的情况下，ACh（0.01-10 microM）引起E +和E-环的剂量依赖性收缩。通过去除内皮或一氧化氮（NO）合酶抑制（N-硝基-L-精氨酸甲酯，P = 0.001）增强ACh收缩。环氧合酶抑制（吲哚美辛）可降低E +和E- PV环中的ACh收缩（分别为P = 0.013和P = 0.037）。 ACh收缩是由电压操作的Ca（2+）通道（硝苯地平，P <0.001），肌醇-1,4,5-三磷酸（IP（3））介导的Ca（2+）释放的抑制剂减弱的（2- E-PV环中的氨基乙氧基二苯基硼酸酯（P = 0.001），PKC（双吲哚基马来酰亚胺I，P = 0.001），Rho激酶（Y-27632，P = 0.002）和酪氨酸激酶（TK; tyrphostin 47，P = 0.015）。 ACh（1 microM）导致[Ca（2 +）]（i）-张力关系（P 0.015）向左移动，即，ACh增加了肌丝Ca（2+）敏感性。 PKC，Rho激酶和TK的抑制作用减弱了ACh诱导的肌丝Ca（2+）敏感性增加（分别为P <0.001，P <0.001和P = 0.024）。这些发现表明，在犬PV中，ACh收缩受NO调节，部分由环氧合酶途径的代谢物介导，并涉及Ca（2+）通过电压操作的Ca（2+）通道和IP（3）介导的Ca（ 2+）版本。此外，ACh诱导增加的肌丝Ca（2+）敏感性，这需要PKC，Rho激酶和TK途径。

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