Effect of Vasoactive Intestinal Peptide on Monkey Prolactin Secretion and Cyclic AMP in Culture: Interaction with Estradiol and Phenol Red

Abstract

To test the hypothesis that estrogenic compounds may decrease the sensitivity of primate lactotropes to adenylate cyclase-mediated secretagogues, the effect of VIP on prolactin secretion and cAMP levels in serum-free monkey pituitary mono-layer cultures was examined in the presence and absence of estradiol (E) and phenol red. In two experimental designs, E treatment was initiated on either the day after dispersion (split plate design) or 10 days after serum-free culture (whole plate design). VIP challenges (5, 50 and 500 nM) were administered for 4 h on days 10 and 20 of culture. There was a significant decrease in the maximal percent stimulation of prolactin by VIP when cultures were treated with E or phenol red. The average percent increase in prolactin at 5, 50 and 500 nM VIP equalled 23, 83 and 156% in the absence of phenol red, but equalled 14, 43 and 112% when E was added to phenol red-free cultures. The percent stimulation by VIP in the presence of phenol red averaged 32, 62 and 97%, but addition of E with phenol red decreased the average stimulation to 26, 45 and 72%, respectively. Basal levels of cAMP were increased by E and phenol red. However, the maximal percent stimulation of cAMP by VIP was decreased in the presence of E and phenol red. In summary, E and phenol red act to decrease the maximal percent stimulation of prolactin secretion by VIP. This effect is reflected by a decrease in the maximal percent stimulation of intracellular cAMP.

Beta-Endorphin, but Not Oxytocin, Substance P or Vasoactive-Intestinal Polypeptide, Contributes to Progesterone-Induced Prolactin Secretion in Monkeys

“…Studies in rats have shown that the suprachiasmatic nucleus (SCN) is the major site of VIP expression [47. 48] and previous maps do not indicate PR in primate SCN [49], However, sever al studies suggested that E + P could stimulate VIP which could in turn stimulate prolactin secretion [24,27,[50][51][52], However, in this study the VIP antagonist had no effect on P-induced prolactin secretion within a physio logical dose range, nor was there a difference in the hypo thalamic content of VIP in the presence or absence of gonadal steroids. Together this data is not consistent with VIP mediating P-induced prolactin release in primates.…”

“…SP stimulates prolactin secretion from hemipituitaries [19] as well as intact and hypothalamic-lesioned rats [20] and monkeys [21]. VIP stimulates the release of prolactin in vivo and in vitro in rats and monkeys [22][23][24][25][26][27], We have documented PR in SP neurons of the arcuate nucleus in macaques [14], but PR have not been reported in VIP neurons. Nonetheless, either SP or VIP could play a role in P-induced prolactin secretion.…”

Lack of vasoactive intestinal peptide-releasing property in prolactin cells from ovariectomized rats: contribution of post-transductional impairments

“…Although the former suggested that oestrogen effects are mediated via changes in Gs proteins, the latter reported a decreased ability of forskolin to stimulate adenylate cyclase following oestrogen treatment, thus implicating also a defect at the level of the enzyme moiety. Finally, in contrast to our evidence, Bethea (28) reported that in primary culture of monkey pituitary cells treated with oestradiol the decreased efficiency of VIP-mediated cyclic AMP production is reflected also in a decrease of PRL secretion. This contrast could be attributed to the different model used, i.e.…”

Lipophilic impurity of phenol red is a potent cation transport modulator

“…Since the first demonstrations of its weak estrogenic activity (Berthois et al, 1986), phenol red attracted much attention (Rajendran et al, 1987;Welshons et al, 1988;Glover et al, 1988;Ernst et al, 1989;Dumesic et al, 1989;Ortmann et al, 1990;Bethea, 1990;Grady et al, 1991;Walsh-Reitz and Toback, 1992). The original findings were confirmed with only one exception (Richards et al, 1988).…”