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α-肾上腺素能受体参与去甲肾上腺素诱导前列腺素E2和促黄体生成素释放激素从中位隆起释放的证据。

Evidence for involvement of alpha-adrenergic receptors in norepinephrine-induced prostaglandin E2 and luteinizing hormone-releasing hormone release from the median eminence.

作者信息

Ojeda S R, Negro-Vilar A, McCann S M

出版信息

Endocrinology. 1982 Feb;110(2):409-12. doi: 10.1210/endo-110-2-409.

Abstract

Studies were conducted to determine if the stimulatory effect that norepinephrine (NE) exerts on the release of prostaglandin E2 (PGE2) and LHRH from the median eminence is mediated by alpha- or beta-adrenergic receptors. Incubation of median eminence fragments from adult male rats with different concentrations of phentolamine, an alpha-receptor antagonist, resulted in a dose-related inhibition of the release of both PGE2 and LHRH induced by NE, with an IC50 of 3.5 X 10(-7) and 0.9 X 10(-7) M for PGE2 and LHRH, respectively. Complete suppression of the NE effects was observed with a phentolamine concentration of 5 X 10(-6) M. This dose also reduced basal PGE2 and LHRH release. In contrast to phentolamine, the beta-receptor antagonist propranolol, tested at a concentration of 5 X 10(-6) M, was completely ineffective in altering the stimulatory effect of NE on either PGE2 or LHRH release. Moreover (and as previously observed for LHRH), blockade of dopaminergic receptors with Pimozide (10(-6) M) failed to inhibit the release of PGE2 induced by NE, thus indicating that the stimulatory effect of NE is not mediated by a dopaminergic mechanism. It is concluded that NE stimulates the release of PGE2 and LHRH from nerve terminals of the median eminence by first interacting with an alpha-adrenergic receptor.

摘要

开展了多项研究以确定去甲肾上腺素(NE)对正中隆起释放前列腺素E2(PGE2)和促性腺激素释放激素(LHRH)的刺激作用是否由α-或β-肾上腺素能受体介导。用不同浓度的α受体拮抗剂酚妥拉明孵育成年雄性大鼠的正中隆起片段,导致NE诱导的PGE2和LHRH释放呈剂量相关抑制,PGE2和LHRH的半数抑制浓度(IC50)分别为3.5×10^(-7)和0.9×10^(-7) M。酚妥拉明浓度为5×10^(-6) M时可完全抑制NE的作用。该剂量也降低了基础PGE2和LHRH的释放。与酚妥拉明相反,浓度为5×10^(-6) M的β受体拮抗剂普萘洛尔在改变NE对PGE2或LHRH释放的刺激作用方面完全无效。此外(如先前对LHRH的观察),用匹莫齐特(10^(-6) M)阻断多巴胺能受体未能抑制NE诱导的PGE2释放,因此表明NE的刺激作用不是由多巴胺能机制介导的。结论是,NE首先与α-肾上腺素能受体相互作用,从而刺激正中隆起神经末梢释放PGE2和LHRH。

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