ABSTRACT

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 μg/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/1 increased (P<0·01) prolactin release from these anterior pituitary cell aggregates. The integrated value for prolactin release was 9·1 ±2·9 ng/10⁷ cells. In the PEP-treated group, basal release of prolactin was greater than that in the control group (P<0·01). However, during exposure to GnRH, the integrated amount of prolactin release by the PEP-treated group (12·5 ± 4·8 ng/10⁷ 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<0·01) increased by GnRH. In contrast, GnRH-stimulated release of prolactin was significantly (P<0·01) suppressed by 100 nmol saralasin/l, a specific AII antagonist, in both control and PEP-treated groups, whereas saralasin did not attenuate GnRH-induced LH release. GnRH-induced LH release was suppressed by PEP treatment during the first 2 min of perifusion, but enhanced throughout the remaining 18 min. In PEP-treated cell aggregates, the release of AI was increased during the later period. These data demonstrate that GnRH is capable of stimulating prolactin release through a mechanism that may involve the release of angiotensin.

Journal of Endocrinology (1990) 125, 225–232

ABSTRACT

The hydrolysis of membrane phosphatidylinositol to yield [³H]labelled inositol phosphates by anterior pituitary cells was stimulated significantly by angiotensin II, TRH and neurotensin over a broad range of concentrations. These secretagogues also stimulated release of prolactin. Although the coincident incubation of dopamine with these agents resulted in a marked diminution of prolactin release, no concomitant reduction in inositol phosphate production was observed. In addition, bromocriptine, a potent agonist of dopamine, also proved ineffective in blunting stimulated phosphatidylinositol catabolism. Although it slightly inhibited basal rates of inositol tris-, bis- and monophosphate production, these results show that the secretagogue-mediated enhancement of phosphatidylinositol catabolism may be correlated with an increased release of prolactin and that the inhibition of hormone release produced by dopamine is not achieved by reducing basal or secretagogue-mediated inositol phosphate production.

J. Endocr. (1986) 110, 389–393