AJP - Endocrinology and Metabolism, Vol 250, Issue 3 288-E295, Copyright © 1986 by American Physiological Society
A possible role of arachidonate metabolism in the mechanism of prolactin release
A. M. Judd, K. Koike and R. M. MacLeod
The cleavage of arachidonate from pituitary phospholipids may contribute to
the process that regulates the release of prolactin. To test this
hypothesis, primary cultures of anterior pituitary cells from female rats
were preincubated with [3H]arachidonate to label their
phospholipid-containing components. The cells were then washed and
incubated with vehicle or test agents and the release into the medium of
prolactin and [3H]arachidonate cleaved from the phospholipids was measured.
Thyrotropin-releasing hormone (TRH) and neurotensin significantly increased
the release of both [3H]arachidonate and prolactin. Although basal
[3H]arachidonate release was not affected by dopamine or somatostatin, both
of these agents reduced [3H]arachidonate release induced by TRH. The
relationship between calcium mobilization and arachidonate release was
investigated by exposing the cells to agents that modify calcium balance.
Maitotoxin, a calcium channel activator, stimulated prolactin and
arachidonate release. In contrast cobalt, a calcium channel blocker,
penfluridol, a calcium-binding protein inhibitor, and low-calcium medium
decreased basal and TRH-induced prolactin release and diminished the
TRH-induced release of arachidonate. RHC 80267, an inhibitor of
diacylglycerol lipase, decreased TRH-induced prolactin and arachidonate
release. BW755c, an inhibitor of the conversion of arachidonate to its
metabolites, decreased TRH-induced prolactin release but predictably
increased arachidonate release. These findings support the hypothesis that
arachidonate metabolites may be involved in the process regulating
prolactin release.
