The experiments will continue investigations into (a) the role of angiotensin II (AII) in the brain in regulating the secretion of luteinizing hormone (LH) and prolactin (PRL) from the anterior pituitary gland and (b) the role of AII synthesized in the adenohypophysis itself in stimulating PRL release. The hypothesis that brain-derived AII affects LH release via brain catecholamines, especially norepinephrine (NE) will be tested in three in vivo systems. The specific alpha receptors involved in the effects of intracerebroventricular AII and NE (1) to suppress pulsatile LH secretion in ovariectomized rats and (2) to stimulate LH release in intact animals on the morning of proestrus will be investigated. In addition, (3) the brain site(s) where AII and NE interact to affect LH and PRL secretion will be studied by measuring changes in catecholamine neuronal activity in specific brain structures during AII administration. Levels of catecholamines and their metabolites will be determined by HPLC in perfusates that have been continuously withdrawn from brain micro-dialysis cannula in conscious rats. The hypothesis that pituitary-derived AII acutely stimulates PRL release will be tested in four in vivo conditions. The effects of AII receptor blockade in the pituitary gland will be studied regarding PRL release in (a) ovariectomized animals, and as a function of stimulation by (b) estradiol, (c) stress and (d) suckling. Results from the studies will confirm that AII, in addition to its well-known effects on cardiovascular function and fluid balance, is intimately involved in reproductive physiology. The connection may be important in the etiology of changes in blood pressure and vascular tone associated with ovarian hormones, i.e. oral contraceptive or pregnancy induced hypertension.
