BLOOD, PITUITARY, AND BRAIN RENIN-ANGIOTENSIN SYSTEMS AND REGULATION OF SECRETION OF ANTERIOR-PITUITARY GLAND

In addition to increasing blood pressure, stimulating aldosterone and vasopressin secretion, and increasing water intake, angiotensin II aff ects the secretion of anterior pituitary hormones. Some of these effec ts are direct. There are angiotensin II receptors on lactotropes and c orticotropes in rats, and there may be receptors on thyrotropes and ot her secretory cells. Circulating angiotensin II reaches these receptor s, but angiotensin II is almost certainly generated locally by the pit uitary renin-angiotensin system as well. There are also indirect effec ts 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-conve rting enzyme. There is debate about whether these cells also contain s mall amounts of angiotensinogen, but most of the angiotensinogen is pr oduced by a separate population of cells and appears to pass in a para crine fashion to the gonadotropes. An analogous situation exists in th e brain. Neurons contain angiotensin II and probably renin, but most a ngiotensin-converting enzyme is located elsewhere and angiotensinogen is primarily if not solely produced by astrocytes. Angiotensin II caus es secretion of prolactin and adrenocorticotropic hormone (ACTH) when added to pituitary cells in vitro. Paracrine regulation of prolactin s ecretion by angiotensin II from the gonadotropes may occur in vitro un der certain circumstances, but the effects of peripheral angiotensin I I on ACTH secretion appear to be mediated via the brain and corticotro pin-releasing hormone (CRH). In the brain, there is good evidence that locally generated angiotensin II causes release of norepinephrine tha t in turn stimulates gonadotropin-releasing hormone-secreting neurons, increasing circulating luteinizing hormone. In addition, there is evi dence that angiotensin II acts in the arcuate nuclei to increase the s ecretion of dopamine into the portal-hypophyseal vessels, inhibiting p rolactin secretion. Central as well as peripheral angiotensin II incre ases CRH secretion, but there is little if any evidence that angiotens in II mediates the ACTH responses to other stressful stimuli.