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去甲肾上腺素和前列腺素E2通过不同的1-α-肾上腺素能受体和前列腺素E2受体刺激大鼠正中隆起释放促性腺激素释放激素。

Noradrenaline and prostaglandin E2 stimulate LH-RH release from rat median eminence through distinct 1-alpha-adrenergic and PGE2 receptors.

作者信息

Heaulme M, Dray F

出版信息

Neuroendocrinology. 1984 Nov;39(5):403-7. doi: 10.1159/000124012.

Abstract

Noradrenaline (NA) and prostaglandin (PG) E2 produced a dose-related stimulation of luteinizing hormone releasing hormone (LH-RH) release from incubated median eminence of adult male rats, with ED50 values of 6.10(-7) and 8.10(-8) M, respectively. The effects of some adrenoceptor agonists (10(-5) M) on LH-RH release were tested: only phenylephrine (alpha 1-agonist) stimulated LH-RH release; clonidine (alpha 2 greater than alpha 1-agonist) and isoproterenol (beta-agonist) were ineffective. Adrenoceptor antagonists (10(-6) M) were also tested: prazosin (alpha 1-antagonist) and phentolamine (alpha 1/alpha 2-antagonist) almost completely suppressed the enhanced release of LH-RH induced by NA. In contrast, neither yohimbine (alpha 2-antagonist) nor propranolol (beta-antagonist) altered this effect of NA. When tested alone, no significant effect was obtained on basal LH-RH release with any of the antagonists tested. Moreover, at concentrations that blocked the stimulation produced by NA, the adrenoceptor antagonists did not alter the effect of PGE2. Among seven PGs tested at 10(-6) M, only PGE2, PGE1, PGA2, and 16,16-dimethyl PGE2 significantly enhanced LH-RH secretion. 8-iso PGE2 weakly stimulated LH-RH secretion, whereas PGF2 alpha and PGD2 were ineffective. A direct correlation existed between the potency of these compounds to modify LH-RH secretion and to inhibit specific [3H]-PGE2 binding to hypothalamic membranes. In conclusion, these results suggest that the stimulation of LH-RH from median eminence induced by NA and PGE2 involves the activation of an alpha 1-adrenergic receptor and a PGE2 receptor, respectively.

摘要

去甲肾上腺素(NA)和前列腺素(PG)E2对成年雄性大鼠离体正中隆起释放促黄体生成激素释放激素(LH-RH)产生剂量相关的刺激作用,其半数有效剂量(ED50)值分别为6×10⁻⁷和8×10⁻⁸ M。测试了一些肾上腺素能受体激动剂(10⁻⁵ M)对LH-RH释放的影响:只有去氧肾上腺素(α1激动剂)刺激LH-RH释放;可乐定(α2>α1激动剂)和异丙肾上腺素(β激动剂)无效。还测试了肾上腺素能受体拮抗剂(10⁻⁶ M):哌唑嗪(α1拮抗剂)和酚妥拉明(α1/α2拮抗剂)几乎完全抑制了NA诱导的LH-RH释放增强。相反,育亨宾(α2拮抗剂)和普萘洛尔(β拮抗剂)均未改变NA的这种作用。单独测试时,所测试的任何一种拮抗剂对基础LH-RH释放均无显著影响。此外,在阻断NA产生的刺激作用的浓度下,肾上腺素能受体拮抗剂并未改变PGE2的作用。在10⁻⁶ M测试的七种PG中,只有PGE2、PGE1、PGA2和16,16-二甲基PGE2显著增强LH-RH分泌。8-异PGE2对LH-RH分泌有微弱刺激作用,而PGF2α和PGD2无效。这些化合物改变LH-RH分泌的能力与抑制特异性[³H]-PGE2与下丘脑膜结合的能力之间存在直接相关性。总之,这些结果表明,NA和PGE2诱导的正中隆起LH-RH刺激分别涉及α1肾上腺素能受体和PGE2受体的激活。

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