Riemer R K, Goldfien A, Roberts J M
Department of Obstetrics-Gynecology and Reproductive Sciences, University of California, San Francisco 94143.
Mol Pharmacol. 1987 Nov;32(5):663-8.
alpha 1-Adrenergic and muscarinic cholinergic stimuli activate uterine contraction. Estrogen increases adrenergic but not cholinergic sensitivity of rabbit myometrium independent of its effects on adrenoceptor concentration. Since both alpha 1-adrenergic and muscarinic receptors are coupled to phosphatidylinositol hydrolysis, we tested the hypothesis that estrogen increases adrenergic- but not cholinergic-mediated inositol triphosphate production. We found that maximal production of inositol phosphates stimulated by norepinephrine was increased approximately 3-fold following estrogen treatment. Cholinergic-stimulated production was not increased by estrogen treatment. These results demonstrate that the effect of estrogen to enhance uterine adrenergic sensitivity is associated with an increased post-receptor response. The nature of the selectivity of estrogen for adrenergic versus cholinergic response remains obscure, but the results suggest the presence of parallel pathways for receptor activation of a common post-receptor response.
α1-肾上腺素能和毒蕈碱胆碱能刺激可激活子宫收缩。雌激素可增加兔子宫肌层的肾上腺素能敏感性，但不增加胆碱能敏感性，这与其对肾上腺素能受体浓度的影响无关。由于α1-肾上腺素能受体和毒蕈碱受体均与磷脂酰肌醇水解偶联，我们检验了雌激素增加肾上腺素能介导而非胆碱能介导的肌醇三磷酸生成这一假说。我们发现，雌激素处理后，去甲肾上腺素刺激的肌醇磷酸最大生成量增加了约3倍。雌激素处理并未增加胆碱能刺激的生成量。这些结果表明，雌激素增强子宫肾上腺素能敏感性的作用与受体后反应增强有关。雌激素对肾上腺素能反应与胆碱能反应选择性的本质仍不清楚，但结果提示存在受体激活共同受体后反应的平行途径。
