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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Inducible nitric oxide synthase is involved in corticotropin-releasing hormone-mediated central sympatho-adrenal outflow in rats.
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Inducible nitric oxide synthase is involved in corticotropin-releasing hormone-mediated central sympatho-adrenal outflow in rats.

机译：诱导型一氧化氮合酶参与促肾上腺皮质激素释放激素介导的大鼠中枢交感-肾上腺流出。

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摘要

Brain nitric oxide (NO), recognized as a neurotransmitter or a neuromodulator, is mainly generated either by neuronal NO synthase (NOS) or by inducible NOS. NO has been shown to activate cyclooxygenase (a prostaglandin-forming enzyme) in addition to guanylate cyclase. Recently, we reported that the intracerebroventricularly (i.c.v.) administered corticotropin-releasing hormone (CRH) increases plasma catecholamines through brain cyclooxygenase-dependent mechanisms in rats. In the present experiments, therefore, we examined whether NO is involved in the CRH-induced increase of plasma catecholamines using urethane-anesthetized rats. I.c.v. administered CRH increased plasma noradrenaline and adrenaline in a dose-dependent manner (0.5, 1.5, and 3.0 nmol/animal). The CRH (1.5 nmol/animal, i.c.v.)-induced increase of plasma catecholamines was reduced by N(omega)-nitro-L-arginine methyl ester (a non-selective inhibitor of NOS) [111 nmol (30 microg)/animal, i.c.v.], but not by the same dose of N(omega)-nitro-D-arginine methyl ester (an inactive isomer of N(omega)-nitro-L-arginine methyl ester). The CRH-induced increase of plasma catecholamines was also reduced either by cycloheximide (an inhibitor of protein synthesis) [107 nmol (30 microg)/animal, i.c.v.] or by S-methylisothiourea (an inhibitor of inducible NOS) [71 nmol (20 microg) and 711 nmol (200 microg)/animal, i.c.v.]. These results suggest the involvement of brain inducible NOS in the CRH-induced activation of the central sympatho-adrenomedullary outflow in rats.
机译：被认为是神经递质或神经调节剂的脑型一氧化氮（NO）主要由神经元NO合酶（NOS）或诱导型NOS产生。已显示除鸟苷酸环化酶外，NO还可以激活环氧合酶（一种前列腺素形成酶）。最近，我们报道，通过大鼠脑中的环氧合酶依赖性机制，脑室内（i.c.v.）给予促肾上腺皮质激素释放激素（CRH）可增加血浆儿茶酚胺。因此，在本实验中，我们使用氨基甲酸乙酯麻醉的大鼠检查了NO是否参与CRH诱导的血浆儿茶酚胺的增加。 I.c.v.给予CRH剂量依赖性（0.5、1.5和3.0 nmol /动物）增加血浆去甲肾上腺素和肾上腺素。 N（ω）-硝基-L-精氨酸甲酯（一种NOS的非选择性抑制剂）[111 nmol（30 microg）/动物， icv]，但剂量不同的N（ω）-硝基-D-精氨酸甲酯（N（ω）-硝基-L-精氨酸甲酯的非活性异构体）。环己酰亚胺（蛋白质合成抑制剂）[107 nmol（30 microg）/动物，icv]或S-甲基异硫脲（诱导型NOS抑制剂）[71 nmol（20） microg）和711 nmol（200 microg）/动物，icv]。这些结果表明，大脑可诱导的NOS参与了CRH诱导的大鼠中央交感神经-肾上腺髓质外流的激活。

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