Ganong W F
Department of Physiology, University of California, San Francisco 94143-0444.
Front Neuroendocrinol. 1993 Jul;14(3):233-49. doi: 10.1006/frne.1993.1008.
In addition to increasing blood pressure, stimulating aldosterone and vasopressin secretion, and increasing water intake, angiotensin II affects the secretion of anterior pituitary hormones. Some of these effects are direct. There are angiotensin II receptors on lactotropes and corticotropes in rats, and there may be receptors on thyrotropes and other secretory cells. Circulating angiotensin II reaches these receptors, but angiotensin II is almost certainly generated locally by the pituitary renin-angiotensin system as well. There are also indirect effects produced by the effects of brain angiotensin II on the secretion of hypophyseotropic hormones. In the anterior pituitary of the rat, the gonadotropes contain renin, angiotensin II, and some angiotensin-converting enzyme. There is debate about whether these cells also contain small amounts of angiotensinogen, but most of the angiotensinogen is produced by a separate population of cells and appears to pass in a paracrine fashion to the gonadotropes. An analogous situation exists in the brain. Neurons contain angiotensin II and probably renin, but most angiotensin-converting enzyme is located elsewhere and angiotensinogen is primarily if not solely produced by astrocytes. Angiotensin II causes secretion of prolactin and adrenocorticotropic hormone (ACTH) when added to pituitary cells in vitro. Paracrine regulation of prolactin secretion by angiotensin II from the gonadotropes may occur in vitro under certain circumstances, but the effects of peripheral angiotensin II on ACTH secretion appear to be mediated via the brain and corticotropin-releasing hormone (CRH). In the brain, there is good evidence that locally generated angiotensin II causes release of norepinephrine that in turn stimulates gonadotropin-releasing hormone-secreting neurons, increasing circulating luteinizing hormone. In addition, there is evidence that angiotensin II acts in the arcuate nuclei to increase the secretion of dopamine into the portal-hypophyseal vessels, inhibiting prolactin secretion. Central as well as peripheral angiotensin II increases CRH secretion, but there is little if any evidence that angiotensin II mediates the ACTH responses to other stressful stimuli.
除了升高血压、刺激醛固酮和血管升压素分泌以及增加水摄入外，血管紧张素II还影响垂体前叶激素的分泌。其中一些作用是直接的。大鼠的促乳素细胞和促肾上腺皮质激素细胞上存在血管紧张素II受体，促甲状腺激素细胞和其他分泌细胞上可能也有受体。循环中的血管紧张素II可到达这些受体，但血管紧张素II几乎肯定也由垂体肾素-血管紧张素系统在局部产生。脑内血管紧张素II对促垂体激素分泌的影响也会产生间接作用。在大鼠垂体前叶中，促性腺激素细胞含有肾素、血管紧张素II和一些血管紧张素转换酶。关于这些细胞是否也含有少量血管紧张素原存在争议，但大多数血管紧张素原是由另一群细胞产生的，似乎以旁分泌方式传递给促性腺激素细胞。脑内也存在类似情况。神经元含有血管紧张素II，可能也含有肾素，但大多数血管紧张素转换酶位于其他部位，血管紧张素原主要（如果不是唯一）由星形胶质细胞产生。体外实验中，血管紧张素II添加到垂体细胞时可导致催乳素和促肾上腺皮质激素（ACTH）分泌。在某些情况下，促性腺激素细胞产生的血管紧张素II对催乳素分泌的旁分泌调节可能在体外发生，但外周血管紧张素II对ACTH分泌的影响似乎是通过脑和促肾上腺皮质激素释放激素（CRH）介导的。在脑内，有充分证据表明局部产生的血管紧张素II会导致去甲肾上腺素释放，进而刺激促性腺激素释放激素分泌神经元，增加循环中的黄体生成素。此外，有证据表明血管紧张素II在弓状核起作用，增加多巴胺向垂体门脉血管的分泌，抑制催乳素分泌。中枢和外周的血管紧张素II都会增加CRH分泌，但几乎没有证据表明血管紧张素II介导ACTH对其他应激刺激的反应。
