Evidence for involvement of an adrenal catecholamine in the beta-adrenergic inhibition of oxytocin release in lactating rats.
Evidence for involvement of an adrenal catecholamine in the beta-adrenergic inhibition of oxytocin release in lactating rats.
复制标题
肾上腺儿茶酚胺参与β-肾上腺素能抑制哺乳大鼠催产素释放的证据。
DOI：
10.1016/0006-8993(88)90700-7
复制
发表时间：
1988
期刊：
影响因子：
2.9
通讯作者：
Grosvenor,CE
中科院分区：
文献类型：
--
作者：
Song,SL;Crowley,WR;Grosvenor,CE
肾上腺素能系统对大鼠催产素（OT）的释放起双重控制作用，α-肾上腺素能受体的刺激使其兴奋，而β-肾上腺素能受体的刺激则抑制了这种神经激素的释放。由于哺乳刺激也会从肾上腺髓质释放肾上腺素，本实验测试了肾上腺源性儿茶酚胺是否可能参与泌乳期间OT释放的肾上腺素能调节。在两个独立的实验中，大鼠在哺乳期中期肾上腺去髓质没有改变基础血浆中OT的水平，但明显增强了哺乳诱导的OT的释放，提示肾上腺儿茶酚胺的抑制作用。异丙肾上腺素刺激β-肾上腺素能受体，可抑制假手术大鼠和肾上腺脱髓大鼠哺乳诱导的OT释放。相反，心得安对β-肾上腺素能受体的阻断阻止了异丙肾上腺素的抑制作用，并且当单独给药时，模拟脱髓调节的作用，以增强哺乳诱导的OT释放。用苯肾上腺素刺激外周α-肾上腺素能受体不影响基础或哺乳诱导的OT释放，但用酚妥拉明阻断α-肾上腺素能受体也完全阻止OT通过哺乳释放。这些数据支持刺激β-肾上腺素能受体抑制OT分泌的概念，并进一步表明，这可能是由于肾上腺儿茶酚胺的作用，它可能集中和/或直接作用于神经垂体。本研究结果还进一步证明，中枢而非外周α-肾上腺素能机制的激活对于哺乳诱导的OT释放是必要的。
Adrenergic systems exert dual control over the release of oxytocin (OT) in rats, with stimulation of α-adrenergic receptors exciting, and stimulation of β-adrenergic receptors inhibiting, release of this neurohormone. Because suckling stimulation also releases epinephrine from the adrenal medulla, the present experiments tested whether catecholamines of adrenal origin may participate in the adrenergic regulation of OT release during lactation. In two independent experiments, adrenal demedullation of rats in midlactation did not alter the basal plasma levels of OT, but makedly enhanced the suckling-induced release of OT, suggesting an inhibitory action of an adrenal catecholamine. The OT release induced by suckling in both sham-operated and adrenal demedullated rats was prevented by stimulation of β-adrenergic receptors with isoproterenol. Conversely, blockade of β-adrenergic receptors with propranolol prevented the inhibitory effects of isoproterenol, and when given alone, mimicked the effects of demedullation to enhance suckling-induced OT release. Stimulation of peripheral α-adrenergic receptors with phenylephrine did not affect either basal or suckling-induced OT release, but blockade of α-adrenergic receptors with phentolamine also completely prevented the release of OT by suckling. These data support the concept that stimulation of β-adrenergic receptors inhibits OT secretion, and further suggest that this may be due, at least in part, to an action of an adrenal catecholamine, which may act centrally and/or directly on the neurohypophysis. The present results also provide further evidence that activation of central, but not peripheral, α-adrenergic mehcanisms is necessary for suckling-induced OT release.