Nitric oxidergic neurogenic vasodilation in the porcine basilar artery.
Nitric oxidergic neurogenic vasodilation in the porcine basilar artery.
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DOI：
10.1159/000158887
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Tony J.-F. Lee;S. Sarwinski
中科院分区：
文献类型：
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作者：
Tony J.-F. Lee;S. Sarwinski
几种物种的脑血管已被证明接受非交感血管扩张神经[15，16]。他们的发射器的性质还没有被确定。在无内皮细胞的孤立脑动脉环中，透壁神经刺激（TNS）诱导的血管扩张未被阿托品或乙啶阻断，表明这些动脉中存在非肾上腺素能、非胆碱能（NANC）血管扩张神经[15，16]。在脑动脉中发现了几种神经肽，如血管活性肠肽和降钙素基因相关肽[4]，这些肽诱导内皮非依赖性血管舒张，这与血管环磷酸腺苷合成增强有关[13]，因此，已被认为是脑血管舒张的潜在递质[3，21]。然而，我们最近的研究结果表明，TNS诱导的猪脑动脉血管舒张不仅与环磷酸腺苷的增加有关，而且与环磷酸鸟苷含量有关。多种递质似乎介导脑神经源性血管舒张[14]。然而，可溶性鸟苷酸环化酶的激活在神经源性血管舒张中起主要作用[14]。激活脑动脉中可溶性鸟苷酸环化酶路径的候选递质仍不清楚。外周[5]和脑[12]血管中内皮介导的扩张已得到证实。有充分的证据表明，内皮源性舒张因子是一氧化氮（NO）或NO释放物质[9，17，19]，其合成的前体是L-精氨酸[9，19]。内皮源性舒张因子或NO通过激活可溶性鸟苷酸环化酶诱导血管舒张[9，20]，其合成被硝基-L-精氨酸和其他精氨酸类似物阻断[9，10，19]。提出NO或NO释放分子介导脑神经源性血管舒张[14]。在本研究中，使用体外组织浴技术在离体脑动脉中检查了这种可能性[15]。我们的研究结果表明，一氧化氮或一氧化氮释放物质介导的主要组成部分，神经源性血管舒张在猪的基础
Cerebral blood vessels from several spe cies have been shown to receive nonsympathetic vasodilator nerves [15, 16]. The na ture of their transmitter has not been posi tively identified. In isolated cerebral arterial rings without endothelial cells, transmural nerve stimulation (TNS) induced vasodila tion was not blocked by atropine or guanethidine, suggesting the presence of nonadrenergic, noncholinergic (NANC) vasodilator nerves in these arteries [15, 16]. Several neural peptides such as vasoac tive intestinal polypeptide and calcitonin gene related peptide have been demon strated in cerebral arteries [4], These pep tides induce an endothelium-independent vasodilation which is associated with an en hanced vascular cyclic adenosine monophos phate synthesis [13] and therefore, have been suggested to be the potential transmitters for cerebral vasodilation [3, 21]. Our recent findings, however, have indicated that TNS-induced vasodilation of pig cerebral arteries is associated with increases not only in cyclic adenosine monphosphate, but also in cyclic guanosine monphosphate contents. Multiple transmitters appear to mediate the cerebral neurogenic vasodilation [14]. Activation of the soluble guanylate cyclase, however, plays a predominant role in the neurogenic vasodi lation [14]. The candidate transmitter for activating the soluble guanylate cyclase path way in the cerebral artery remains un known.The endothelium-mediated dilations in peripheral [5] and cerebral [12] blood vessels are well established. There is good evidence that the endothelium-derived relaxing factor is nitric oxide (NO) or a NO-releasing sub stance [9, 17, 19] and that the precursor from which it is synthesized is L-arginine [9, 19]. Endothelium-derived relaxing factor or NO induces vasodilation by activating soluble guanylate cyclase [9, 20], and its synthesis is blocked by nitro-L-arginine and other argi nine analogues [9, 10, 19]. NO or a NO-releasing molecule was proposed to mediate cerebral neurogenic vasodilation [14]. This possibility was examined in isolated cerebral arteries in the present study, using an in vitro tissue bath technique [15]. Our results demonstrate that NO or a NO-releasing sub stance mediates a major component of the neurogenic vasodilation in the porcine basi