The paracrine role of angiotensin in gonadotrophin-releasing hormone-stimulated prolactin release in rats.

It is well known that lactotrophs are in close proximity to gonadotrophs in the lateral region of the pituitary gland, and thus there is interest in interactions between these two types of cell. The present study was undertaken to investigate the role of angiotensin II (AII) in gonadotrophin-releasing hormone (GnRH)-induced prolactin release, and to examine the effect of oestradiol on the paracrine interaction among anterior pituitary cells of young male rats. Over a 3-day period, one group of rats was injected twice with polyoestradiol phosphate (0.5 microgram/g body weight; PEP-treated group), and a second with saline (control group). Their anterior pituitary glands were enzymatically dispersed and, subsequently, the cells were allowed to reaggregate for 48 h. A 20-min perifusion with 100 nmol GnRH/l increased (P less than 0.01) prolactin release from these anterior pituitary cell aggregates. The integrated value for prolactin release was 9.1 +/- 2.9 ng/10(7) cells. In the PEP-treated group, basal release of prolactin was greater than that in the control group (P less than 0.01). However, during exposure to GnRH, the integrated amount of prolactin release by the PEP-treated group (12.5 +/- 4.8 ng/10(7) cells) was not significantly different from that of the control group, although in each individual experiment the GnRH-stimulated prolactin release from the PEP-treated cells was higher than that from the cells that had not been exposed to PEP. The release of angiotensin I (AI) from these perifused pituitary aggregates was significantly (P less than 0.01) increased by GnRH.(ABSTRACT TRUNCATED AT 250 WORDS)