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多巴胺能受体的外周调节影响大鼠的勃起反应。

Peripheral modulation of dopaminergic receptors affects erectile responses in rats.

作者信息

El-Din Mahmoud Mohy, Senbel Amira M, Daabees Tahia T, Sharabi Fouad M

机构信息

Department of Pharmacology, Faculty of Pharmacy, University of Alexandria, Alexandria, Egypt.

出版信息

Basic Clin Pharmacol Toxicol. 2007 Apr;100(4):225-32. doi: 10.1111/j.1742-7843.2006.00013.x.

Abstract

Clinical observations have suggested that dopaminergic mechanisms are involved in the regulation of male sexual responses, including erection. Apomorphine was initially reported to exert its erectogenic effects by modifying central dopaminergic activity. This study aimed primarily at evaluating and investigating the effect of apomorphine on erectile functions in rats and its potential effects on the cardiovascular system, as well as the possible role of dopaminergic stimulation in the peripheral control of erection. Measurement of intracavernosal pressure changes elicited by electrical stimulation of the cavernosal nerve in anaesthetized rats and mating tests were used. SCH23390, the D1 receptor antagonist, attenuated penile response to electrical stimulation. Intravenous administration of apomorphine in low dose (100 microg/kg), but not in high dose, significantly potentiated erectile responses to electrical stimulation. Intracavernosally injected apomorphine (50 microg/kg) significantly potentiated the filling rate of the corpora cavernosa 5 min. after injection, and did not induce erection in absence of electrical stimulation. In addition, apomorphine amplified the male sexual and copulatory behaviour by reducing ejaculation, mount and intromission latencies, and significantly increasing the number of ejaculations per session. However, apomorphine produced rapid and long-lasting hypotension and potentiated the hypotension and tachycardia associated with nerve-stimulated penile erection. Our results suggest that D1-dopaminergic receptors may be functionally involved in the peripheral mediation of penile erection. Apomorphine may amplify sexual and copulatory behaviour and may also, by a complementary role, amplify neurogenically mediated erections by acting in the periphery.

摘要

临床观察表明,多巴胺能机制参与男性性反应的调节,包括勃起。最初有报道称,阿扑吗啡通过改变中枢多巴胺能活性发挥其勃起作用。本研究主要旨在评估和研究阿扑吗啡对大鼠勃起功能的影响及其对心血管系统的潜在作用,以及多巴胺能刺激在勃起外周控制中的可能作用。采用了对麻醉大鼠海绵体神经进行电刺激引发的海绵体内压力变化测量以及交配试验。D1受体拮抗剂SCH23390减弱了阴茎对电刺激的反应。静脉注射低剂量(100微克/千克)而非高剂量的阿扑吗啡,可显著增强对电刺激的勃起反应。海绵体内注射阿扑吗啡(50微克/千克)在注射后5分钟可显著增强海绵体的充盈率,且在无电刺激时不会诱发勃起。此外,阿扑吗啡通过缩短射精、爬跨和插入潜伏期,并显著增加每次性交射精次数,增强了雄性性行为和交配行为。然而,阿扑吗啡会产生快速且持久的低血压,并增强与神经刺激阴茎勃起相关的低血压和心动过速。我们的结果表明,D1多巴胺能受体可能在阴茎勃起的外周介导中发挥功能作用。阿扑吗啡可能增强性行为和交配行为,并且还可能通过在外周发挥作用,以互补的方式增强神经源性介导的勃起。

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