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首页> 外文期刊>Pharmacology and Toxicology: An International Journal >Phenylephrine induces endogenous noradrenaline release in the rat vas deferens through nitric oxide synthase pathway.
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Phenylephrine induces endogenous noradrenaline release in the rat vas deferens through nitric oxide synthase pathway.

机译：苯肾上腺素通过一氧化氮合酶途径诱导大鼠输精管内源性去甲肾上腺素释放。

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We have previously observed that in the rat vas deferens nitric oxide synthase pathway potentiated phenylephrine-induced contractility raising the possibility of a facilitatory role on neurotransmission by nitric oxide. To confirm this hypothesis we studied the effect of phenylephrine on the concentration response curves obtained in preparations from reserpine-treated rats in the absence and presence of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA). The endogenous noradrenaline released by normal preparations (without reserpine) was measured in the perfusion fluid of preparations stimulated with phenylephrine, in the absence and presence of L-NMMA, L-NMMA + the nitric oxide donor 3-morpholinosydnonimine hydrochloride (SIN-1), the alpha1-adrenoceptor antagonist prazosin and the blocker of noradrenaline carrier desipramine. The phenylephrine-induced noradrenaline release in a calcium-free medium was also measured. L-NMMA decreased the Emax of phenylephrine concentration response curves obtained in preparations from normal (reserpine-untreated) but not from reserpine-treated rats. In the perfusion fluid of preparations incubated with phenylephrine, a concentration-dependent increase of noradrenaline was observed which was reversed by L-NMMA and restored when SIN-1 was added together with the nitric oxide synthase inhibitor. The concentration-dependent phenylephrine-induced noradrenaline increase was not modified by desipramine but was abolished by 10 microM prazosin. In calcium-free medium, phenylephrine failed to increase the noradrenaline concentration. These results suggest that in the rat vas deferens, nitric oxide pathway potentiates the phenylephrine-induced contractility through a mechanism which involves calcium-dependent release of endogenous noradrenaline and seems to depend, at least partially on the activation of alpha1-adrenoceptors.
机译：我们以前已经观察到在大鼠输精管中一氧化氮合酶途径增强了去氧肾上腺素诱导的收缩性，增加了一氧化氮对神经传递的促进作用的可能性。为了证实该假设，我们研究了在没有一氧化氮合酶抑制剂NG-单甲基-L-精氨酸（L-NMMA）的情况下，去氧肾上腺素对从利血平治疗的大鼠制剂中获得的浓度响应曲线的影响。在不存在和存在L-NMMA，L-NMMA +一氧化氮供体3-盐酸吗啉代亚胺盐酸盐（SIN-1）的情况下，在用去氧肾上腺素刺激的制剂的灌注液中测量了正常制剂（无利血平）释放的内源性去甲肾上腺素，α1-肾上腺素能受体拮抗剂哌唑嗪和去甲肾上腺素载体地昔帕明的阻滞剂。还测量了去氧肾上腺素诱导的去甲肾上腺素在无钙培养基中的释放。 L-NMMA降低了从正常（未经利血平治疗的）制剂中获得的去氧肾上腺素浓度响应曲线的Emax，但未从经利血平治疗的大鼠中获得。在与去氧肾上腺素一起温育的制剂的灌注液中，观察到去甲肾上腺素的浓度依赖性增加，其被L-NMMA逆转并且当与一氧化氮合酶抑制剂一起添加SIN-1时得以恢复。浓度依赖的去氧肾上腺素诱导的去甲肾上腺素增加没有被地昔帕明改变，但被10 microM哌唑嗪消除了。在无钙培养基中，去氧肾上腺素不能增加去甲肾上腺素的浓度。这些结果表明在大鼠输精管中，一氧化氮途径通过一种机制增强了去氧肾上腺素诱导的收缩性，该机制涉及钙依赖性释放内源性去甲肾上腺素，并且似乎至少部分取决于α1-肾上腺素受体的激活。

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