al-Damluji S
National Institute of Neurological Diseases, National Institute of Health, Bethesda, MD 20892.
Baillieres Clin Endocrinol Metab. 1993 Apr;7(2):355-92. doi: 10.1016/s0950-351x(05)80180-6.
The hypothalamic hypophysiotrophic neurones are densely innervated by adrenergic and noradrenergic nerve terminals. Activation of alpha 1-adrenoceptors located in the brain stimulates the secretion of ACTH, prolactin and TSH. The effects of the alpha 1-adrenoceptors seem to be exerted on hypothalamic neurones that secrete vasopressin, CRH-41 and TRH. These mechanisms are important in the physiological control of the secretion of ACTH and TSH in humans. alpha 2-Adrenoceptors are not involved in the control of secretion of these hormones under basal conditions in humans. However, alpha 2-adrenoceptors exert an inhibitory effect that acts as a negative feedback mechanism, limiting excessive secretion of these hormones. There is no convincing evidence for the involvement of beta-adrenoceptors in the control of the secretion of these three hormones in humans. Studies on cultured anterior pituitary cells suggested that adrenaline and noradrenaline may influence the secretion of ACTH, prolactin and TSH directly at the level of the pituitary. However, these effects are not demonstrable in humans, and are likely to be due to alterations in the pituitary adrenoceptors during culture. In the case of growth hormone, activation of alpha 2-adrenoceptors located in the brain stimulates secretion of this hormone both by increasing the secretion of GHRH and by inhibiting the secretion of somatostatin. Activation of beta-adrenoceptors inhibits the secretion of growth hormone via an increase in the secretion of somatostatin. The effects of the central alpha 2- and beta-adrenoceptors are important in the physiological control of growth hormone secretion in humans. A considerable amount of evidence implicates brain alpha 1-adrenoceptors in the control of secretion of the gonadotrophins in experimental animals, but, despite intensive study, no convincing evidence has been found in humans of reproductive age.
下丘脑促垂体神经元受到肾上腺素能和去甲肾上腺素能神经末梢的密集支配。位于脑内的α1肾上腺素能受体激活可刺激促肾上腺皮质激素（ACTH）、催乳素和促甲状腺激素（TSH）的分泌。α1肾上腺素能受体的作用似乎是通过作用于分泌血管加压素、促肾上腺皮质激素释放激素（CRH-41）和促甲状腺激素释放激素（TRH）的下丘脑神经元来实现的。这些机制在人体ACTH和TSH分泌的生理调节中很重要。在人体基础状态下，α2肾上腺素能受体不参与这些激素分泌的调控。然而，α2肾上腺素能受体发挥抑制作用，作为一种负反馈机制，限制这些激素的过度分泌。没有令人信服的证据表明β肾上腺素能受体参与人体这三种激素分泌的调控。对培养的垂体前叶细胞的研究表明，肾上腺素和去甲肾上腺素可能在垂体水平直接影响ACTH、催乳素和TSH的分泌。然而，这些作用在人体中无法得到证实，可能是由于培养过程中垂体肾上腺素能受体发生了改变。就生长激素而言，位于脑内的α2肾上腺素能受体激活可通过增加生长激素释放激素（GHRH）的分泌和抑制生长抑素的分泌来刺激该激素的分泌。β肾上腺素能受体激活通过增加生长抑素的分泌来抑制生长激素的分泌。中枢α2和β肾上腺素能受体的作用在人体生长激素分泌的生理调节中很重要。大量证据表明，脑内α1肾上腺素能受体在实验动物促性腺激素分泌的调控中起作用，但尽管进行了深入研究，在育龄人体中尚未找到令人信服的证据。
