Vasoactive intestinal peptide increases the liberation of arachidonate from anterior pituitary cells in vitro.

Several secretagogues increase prolactin (PRL) release from anterior pituitary cells through biochemical pathways that involve the liberation of arachidonate from cellular phospholipids. Vasoactive intestinal peptide (VIP) increases PRL release from anterior pituitary cells through a mechanism involving the generation of cAMP. In this study, we determined whether VIP increases the liberation of arachidonate from anterior pituitary cells. Primary cultures of anterior pituitary cells were prepared from the anterior pituitary gland of female Sprague-Dawley rats. After four to five days in culture, the incubation medium was replaced with [3H] arachidonate containing medium, and the cells incubated for 90 min. The cells were then extensively rinsed with incubation medium without [3H] arachidonate to remove the [3H] fatty acid not associated with cellular phospholipids. The pituitary cells were then incubated with medium containing various concentrations of VIP and the release of [3H] arachidonate and PRL into the incubation medium determined. VIP (500 nM) significantly increased [3H] arachidonate liberation from primary cultures of anterior pituitary cells at 30 min (p < 0.5) and 60 min (p < 0.01), but had no significant effect on the liberation of this fatty acid at 15 or 120 min. PRL release was significantly increased by VIP at 30, 60, and 120 min. VIP (60 min exposure) at concentrations of 100 and 500 nM significantly increased PRL release and arachidonate liberation in a concentration-dependent manner. Similarly, VIP increased [3H] arachidonate liberation from a preparation of anterior pituitary cells enriched in lactotropes. Since the increment in [3H] arachidonate liberation was greater in the lactotrope-enriched population than in the anterior pituitary cell preparation, it is highly probable that the lactotropes are the primary source of [3H] arachidonate liberated by VIP. These experiments provide evidence that [3H] arachidonate liberation may play a role in VIP-stimulated PRL release.