Evidence that nitric oxide can act centrally to stimulate vasopressin release.
Evidence that nitric oxide can act centrally to stimulate vasopressin release.
复制标题
有证据表明一氧化氮可以集中刺激加压素的释放。
DOI：
10.1159/000126459
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发表时间：
1993
影响因子：
4.1
通讯作者：
Share,L
中科院分区：
文献类型：
--
作者：
Ota,M;Crofton,JT;Festavan,GT;Share,L
一氧化氮（NO）是内皮源性舒张因子，可引起血管平滑肌舒张。NO合成酶是由其前体L-精氨酸合成NO的酶，也广泛分布于脑中的神经元中，并且已经表明NO可能充当重要的神经调节剂。由于NO合成酶是目前在下丘脑在相对较高的浓度，我们已经确定是否NO可以影响释放加压素在清醒的，长期准备大鼠。脑室内（i. c. v.）注射S-亚硝基-N-乙酰青霉胺（12.5和25 μg; SNAP），自发分解形成NO，分别引起血浆加压素浓度短暂剂量相关性增加1和2 μU/ml（p < 0.01）。在对照实验中，静脉注射制备SNAP的前体N-乙酰青霉胺（25 μg），血浆加压素水平小幅增加（0.4 μU/ml）（p < 0.01）。静脉注射L-精氨酸（0.5和1毫克），也是NO生物合成的前体，导致血浆加压素浓度的剂量依赖性增加，其幅度与SNAP引起的相似。当静脉注射不能作为NO合成酶底物的D-精氨酸（1 mg）时，血浆血管加压素浓度仅有轻微延迟的增加。因此，NO可以中枢作用以刺激加压素释放，并且可以作为控制加压素释放的神经调节剂。
Nitric oxide (NO) is the endothelium-derived relaxing factor, which causes relaxation of vascular smooth muscle. NO synthetase, the enzyme for the synthesis of NO from its precursor L-arginine, is also widely distributed in neurons in the brain, and it has been suggested that NO may serve as an important neuromodulator. Because NO synthetase is present in the hypothalamus in relatively high concentration, we have determined whether NO can affect the release of vasopressin in conscious, chronically prepared rats. The intra-cerebroventricular (i.c.v.) injection of S-nitroso-N-acetylpenicillamine (12.5 and 25 µg; SNAP), that spontaneously breaks down to form NO, caused transient dose-related increases in the plasma vasopressin concentration of 1 and 2 µU/ml (p < 0.01), respectively. In control experiments in which N-ace-tylpenicillamine (25 µg), the precursor for the preparation of SNAP, was injected i.c.v. there was a small, 0.4 µU/ml, increase (p < 0.01) in the plasma vasopressin level. The i.c.v. injection of L-arginine (0.5 and 1 mg), also the precursor for the biosynthesis of NO, resulted in dose-dependent increases in the plasma vasopressin concentration similar in magnitude to those caused by SNAP. When D-arginine (1 mg), which cannot serve as a substrate for NO synthetase, was injected i.c.v., there was only a slight delayed increase in the plasma vasopressin concentration. Thus, NO can act centrally to stimulate vasopressin release and may serve as a neuromodulator in the control of vasopressin release.