Trachte G J
Department of Pharmacology, University of Minnesota-Duluth, Medical School, 55812.
Prostaglandins. 1988 Aug;36(2):215-28. doi: 10.1016/0090-6980(88)90308-5.
The role of prostaglandins in mediating angiotensin effects on autonomic neurotransmission was assessed. This was accomplished by examining the angiotensin-induced production of prostaglandins (PGE) and suppression of non-adrenergic (purinergic) neurotransmission in the presence and absence of cyclo-oxygenase inhibitors. The vas deferens of the rabbit was utilized for these studies because this preparation has a predominant non-adrenergic neurogenic component. Both angiotensins II and III enhanced PGE production and reduced non-adrenergic neurogenic contractions in a concentration-dependent manner from 1 to 1000 nM. Furthermore, indomethacin (2.8 microM) and eicosatetraynoic acid (10 microM) eliminated the inhibitory effect of the angiotensins on non-adrenergic neurotransmission. However, acetylsalicylic acid (10 microM) prevented the production of PGE in response to the angiotensins but failed to alter the suppression of non-adrenergic neurotransmission. The latter data are inconsistent with the hypothesis that PG's mediate angiotensin-induced depression of non-adrenergic neurotransmission. The mechanism by which indomethacin and eicosatetraynoic acid prevent angiotensin effects on non-adrenergic neurotransmission was not elucidated but previous reports suggest that these agents may act as angiotensin receptor antagonists. All of the cyclo-oxygenase inhibitors examined tended to potentiate angiotensin effects on adrenergic neurotransmission.
评估了前列腺素在介导血管紧张素对自主神经传递作用中的角色。这是通过在存在和不存在环氧化酶抑制剂的情况下，检测血管紧张素诱导的前列腺素（PGE）生成以及对非肾上腺素能（嘌呤能）神经传递的抑制来实现的。本研究使用了兔输精管，因为该标本具有主要的非肾上腺素能神经源性成分。血管紧张素II和III均以浓度依赖的方式（从1到1000 nM）增强了PGE的生成，并减少了非肾上腺素能神经源性收缩。此外，吲哚美辛（2.8 microM）和二十碳四烯酸（10 microM）消除了血管紧张素对非肾上腺素能神经传递的抑制作用。然而，乙酰水杨酸（10 microM）可阻止血管紧张素诱导的PGE生成，但未能改变对非肾上腺素能神经传递的抑制作用。后一组数据与前列腺素介导血管紧张素诱导的非肾上腺素能神经传递抑制这一假说不一致。吲哚美辛和二十碳四烯酸阻止血管紧张素对非肾上腺素能神经传递作用的机制尚未阐明，但先前的报告表明，这些药物可能作为血管紧张素受体拮抗剂起作用。所检测的所有环氧化酶抑制剂均倾向于增强血管紧张素对肾上腺素能神经传递的作用。
