NITRIC-OXIDE IS A POTENT RELAXANT OF HUMAN AND RABBIT CORPUS CAVERNOSUM
NITRIC-OXIDE IS A POTENT RELAXANT OF HUMAN AND RABBIT CORPUS CAVERNOSUM
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DOI：
10.1016/s0022-5347(17)37671-1
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发表时间：
1992-06-01
影响因子：
6.6
通讯作者：
IGNARRO, LJ
中科院分区：
文献类型：
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作者：
BUSH, PA;ARONSON, WJ;IGNARRO, LJ
一氧化氮 (NO) 可使从人类和兔子身上分离出来的预先收缩的海绵体带产生有效、显着和短暂的松弛。 NO 引起的松弛反应与通过非肾上腺素能-非胆碱能途径的电场刺激引起的松弛非常相似。 硝普钠、硝化甘油和 S-亚硝基-N-乙酰青霉胺是已知会产生 NO 的硝基血管扩张剂，也会引起海绵体明显的浓度依赖性松弛。 环 GMP 磷酸二酯酶抑制剂 M&B 22,948 增强了对 NO 的松弛反应，并被氧合血红蛋白抑制。 类似地，M&B 22,948 增强了海绵体对电场刺激或乙酰胆碱的松弛反应，并被氧合血红蛋白抑制。 NO 刺激海绵体中环 GMP 的形成，并且发现松弛程度与环 GMP 形成之间存在密切的正相关性。 数据表明，NO 引起的鸟苷酸环化酶激活和环 GMP 形成代表了负责松弛和非肾上腺素能-非胆碱能介导的阴茎勃起的信号转导机制。 这些观察结果表明，NO 是人和兔海绵体的有效松弛剂，并支持我们的假设，即内源性 NO 是由非肾上腺素能-非胆碱能刺激引起的阴茎勃起的主要介质。
Nitric oxide (NO) caused a potent, marked, and transient relaxation of precontracted strips of corpus cavernosum isolated from humans and rabbits. The relaxation response elicited by NO was very similar to the relaxation evoked by electrical field stimulation via the nonadrenergic-noncholinergic pathway. Sodium nitroprusside, nitroglycerin, and S-nitroso-N-acetylpenicillamine, which are nitrovasodilators known to generate NO, also caused marked concentration-dependent relaxation of corpus cavernosum. Relaxant responses to NO were enhanced by the cyclic GMP phosphodiesterase inhibitor M&B 22,948 and inhibited by oxyhemoglobin. Similarly, relaxation of corpus cavernosum in response to electrical field stimulation or acetylcholine was enhanced by M&B 22,948 and inhibited by oxyhemoglobin. NO stimulated cyclic GMP formation in corpus cavernosum and a close positive correlation was found between the magnitudes of relaxation and cyclic GMP formation. The data suggest that NO-elicited activation of guanylate cyclase and cyclic GMP formation represents the signal transduction mechanism responsible for relaxation and nonadrenergic-noncholinergic-mediated penile erection. These observations indicate that NO is a potent relaxant of human and rabbit corpus cavernosum and support our hypothesis that endogenous NO is the principal mediator of penile erection caused by nonadrenergic-noncholinergic stimulation.