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首页> 外文期刊>American Journal of Physiology >Nitric oxide relaxes human myometrium by a cGMP-independent mechanism.
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Nitric oxide relaxes human myometrium by a cGMP-independent mechanism.

机译：一氧化氮通过cGMP独立机制使人子宫肌层松弛。

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摘要

The role of intracellular guanosine 3',5'-cyclic monophosphate concentration ([cGMP]i) in nitric oxide (NO)-mediated relaxations in the uterus has become controversial. We found the NO donor S-nitroso-L-cysteine (CysNO) to potently (IC50 = 30 nM) inhibit spontaneous contractions in the nonpregnant human myometrium. CysNO treatment increased [cGMP]i significantly (P < 0.001), and this increase was blocked by the guanylyl cyclase inhibitors methylene blue (10 microM) or LY-83583 (1 microM); however, pretreatment with these guanylyl cyclase inhibitors failed to block CysNO-mediated relaxations. Intracellular cAMP concentrations were not altered by treatment of tissues with 10 microM CysNO. Incubation with the cGMP analogs 8-bromo-cGMP or beta-phenyl-1,N2-etheno-cGMP did not significantly affect spontaneous contractility. Pretreatment of tissues with charybdotoxin [a calcium-dependent potassium channel (BK) blocker] completely reversed CysNO-induced relaxations. We conclude that NO is a potent inhibitor of spontaneous contractile activity in the nonpregnant human uterus and that, although guanylyl cyclase and BK activities are increased by NO, increases in [cGMP]i are not required for NO-induced relaxations in this tissue.
机译：细胞内鸟苷3'，5'-环一磷酸浓度（[cGMP] i）在一氧化氮（NO）介导的子宫松弛中的作用已引起争议。我们发现NO供体S-亚硝基-L-半胱氨酸（CysNO）可以有效地（IC50 = 30 nM）抑制人非子宫肌层的自发性收缩。 CysNO处理可显着提高[cGMP] i（P <0.001），而这一增加被鸟苷酸环化酶抑制剂亚甲基蓝（10 microM）或LY-83583（1 microM）所阻止;但是，用这些鸟苷酰环化酶抑制剂进行的预处理未能阻止CysNO介导的松弛。通过用10 microM CysNO处理组织不会改变细胞内cAMP的浓度。与cGMP类似物8-bromo-cGMP或β-苯基-1，N2-乙烯-cGMP一起孵育不会显着影响自发收缩力。用Charybdotoxin（一种钙依赖性钾通道（BK）阻滞剂）预处理组织可以完全逆转CysNO诱导的松弛。我们得出结论，NO是非妊娠人子宫自发收缩活性的有效抑制剂，并且尽管NO可以提高鸟苷酸环化酶和BK的活性，但NO诱导的该组织松弛不需要[cGMP] i的增加。

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