Ojeda S R, Negro-Vilar A, McCann S M
Endocrinology. 1982 Feb;110(2):409-12. doi: 10.1210/endo-110-2-409.
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.
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。
