Role of angiotensin on paracrine prolactin release in the pituitary gland and its possible effects on ovarian function.

The present study was undertaken to investigate the role of angiotensin II (AII) in GnRH-induced PRL release on the paracrine interaction among anterior pituitary cells of young male rats. A 20-min perifusion with 100 nM GnRH increased PRL release (p less than 0.01) from pituitary cell aggregates, and GnRH-stimulated release of PRL was significantly suppressed by saralasin, a specific AII antagonist. The release of AI from pituitary cell aggregates was significantly (p less than 0.01) increased by GnRH. These data demonstrate that GnRH is capable of stimulating PRL release through a mechanism that may involve the release of angiotensin. It was also speculated that some factors released from pituitary cells, such as angiotensin, might be involved in the control of ovarian functions. As an approach to investigate this possibility, porcine anterior pituitary cells and ovarian granulosa cells were co-cultured on type 1 collagen membrane which permits the exchange of the substance with molecular weights less than 9,000. The growth and progesterone production of the granulosa cells co-cultured with pituitary cells were significantly (p less than 0.05) greater than those of the cells cultured in monolayer fashion. Thus, the results of the present study revealed the biological significances of the paracrine system involving angiotensin between gonadotroph and lactotroph in pituitary cells and the direct effect of the factors derived from pituitary cells on ovarian functions.