Song S L, Crowley W R, Grosvenor C E
Department of Physiology and Biophysics, University of Tennessee, Memphis, College of Medicine 38163.
Brain Res. 1988 Aug 9;457(2):303-9. doi: 10.1016/0006-8993(88)90700-7.
Adrenergic systems exert dual control over the release of oxytocin (OT) in rats, with stimulation of alpha-adrenergic receptors exciting, and stimulation of beta-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 markedly 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 beta-adrenergic receptors with isoproterenol. Conversely, blockade of beta-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 alpha-adrenergic receptors with phenylephrine did not affect either basal or suckling-induced OT release, but blockade of alpha-adrenergic receptors with phentolamine also completely prevented the release of OT by suckling. These data support the concept that stimulation of beta-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, alpha-adrenergic mechanisms is necessary for suckling-induced OT release.
肾上腺素能系统对大鼠催产素（OT）的释放发挥双重控制作用，刺激α-肾上腺素能受体会促进这种神经激素的释放，而刺激β-肾上腺素能受体则会抑制其释放。由于哺乳刺激也会促使肾上腺髓质释放肾上腺素，因此本实验旨在测试源自肾上腺的儿茶酚胺是否可能参与哺乳期OT释放的肾上腺素能调节。在两项独立实验中，处于哺乳期中期的大鼠进行肾上腺髓质摘除术并未改变OT的基础血浆水平，但显著增强了哺乳诱导的OT释放，这表明肾上腺儿茶酚胺具有抑制作用。用异丙肾上腺素刺激β-肾上腺素能受体可阻止假手术组和肾上腺髓质摘除组大鼠由哺乳诱导的OT释放。相反，用普萘洛尔阻断β-肾上腺素能受体可阻止异丙肾上腺素的抑制作用，并且单独给予时，其模拟了髓质摘除的效果，增强了哺乳诱导的OT释放。用去氧肾上腺素刺激外周α-肾上腺素能受体对基础或哺乳诱导的OT释放均无影响，但用酚妥拉明阻断α-肾上腺素能受体也完全阻止了哺乳引起的OT释放。这些数据支持了刺激β-肾上腺素能受体会抑制OT分泌的观点，并进一步表明这可能至少部分归因于肾上腺儿茶酚胺的作用，其可能在中枢起作用和/或直接作用于神经垂体。本研究结果还提供了进一步的证据，即中枢而非外周α-肾上腺素能机制的激活是哺乳诱导OT释放所必需的。
