Shi C Z, Zhuang L Z
State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing.
Life Sci. 1993;52(20):1657-65. doi: 10.1016/0024-3205(93)90048-8.
Norepinephrine (NE) was investigated for its effect on progesterone secretion from 6-8 week gestation human trophoblast tissue cultured in serum-free medium. Norepinephrine (5 micrograms/ml) enhanced progesterone secretion significantly on the third day of treatment. The stimulatory effect of NE on progesterone production was abolished by the alpha 1-receptor specific antagonist prazosin (10(-4) M) (P < 0.05), but was not influenced by the alpha 2-receptor specific antagonist yohimbine (10(-4) M) and the beta 1-receptor specific antagonist atenolol (10(-4) M). On the other hand, the alpha-receptor agonist clonidine (10(-6) M) had a similar stimulatory effect on progesterone release but the effect was antagonized by both the alpha 1-antagonist prazosin and the alpha 2-antagonist yohimbine. Further study showed that NE induced a significant increase in cyclic adenosine monophosphate (cAMP) production by trophoblast tissue. Cyclic AMP secretion in the NE treated group was fivefold higher than that of the control group. The effect of NE was blocked by the voltage-dependent calcium channel blocker nifedipine (100 microM) but not by the voltage-independent calcium channel blocker gadolinium chloride (GdCl3) (10 microM). In addition, anti-gonadotropin releasing hormone (GnRH) IgG (5 micrograms/ml) and GnRH antagonist, (D-Phe2, D-Trp6)-GnRH (10(-6) M) did not influence the stimulatory effect of NE on progesterone release. The results indicate that NE regulates progesterone production in human first trimester trophoblast tissue. The effect of NE was mediated by the alpha 1 receptors. Cyclic AMP and voltage-dependent calcium channel were involved in its action.
研究了去甲肾上腺素（NE）对在无血清培养基中培养的6 - 8周妊娠人滋养层组织孕酮分泌的影响。去甲肾上腺素（5微克/毫升）在处理的第三天显著增强了孕酮分泌。NE对孕酮产生的刺激作用被α1受体特异性拮抗剂哌唑嗪（10⁻⁴ M）消除（P < 0.05），但不受α2受体特异性拮抗剂育亨宾（10⁻⁴ M）和β1受体特异性拮抗剂阿替洛尔（10⁻⁴ M）的影响。另一方面，α受体激动剂可乐定（10⁻⁶ M）对孕酮释放有类似的刺激作用，但该作用被α1拮抗剂哌唑嗪和α2拮抗剂育亨宾均拮抗。进一步研究表明，NE诱导滋养层组织中环磷酸腺苷（cAMP）产生显著增加。NE处理组的cAMP分泌比对照组高五倍。NE的作用被电压依赖性钙通道阻滞剂硝苯地平（100微摩尔）阻断，但不被电压非依赖性钙通道阻滞剂氯化钆（GdCl₃）（10微摩尔）阻断。此外，抗促性腺激素释放激素（GnRH）IgG（5微克/毫升）和GnRH拮抗剂（D - Phe²，D - Trp⁶）- GnRH（10⁻⁶ M）不影响NE对孕酮释放的刺激作用。结果表明，NE调节人孕早期滋养层组织中的孕酮产生。NE的作用由α1受体介导。cAMP和电压依赖性钙通道参与其作用。
