Cellular mechanisms by which oxytocin mediates uterine prostaglandin F2α synthesis in bovine endometrium:: Role of calcium

The objective of these experiments was to determine the role of Ca2+ during oxytocin-stimulated prostaglandin (PG) F-2 alpha release from bovine endometrial tissue in vitro. Uteri were collected from dairy cows on the day after spontaneous luteal regression. Caruncular endometrial explants were dissected and incubated in vitro to determine phospholipase C activity or PGF(2 alpha) release. A23187 (a calcium ionophore) and maitotoxin tan activator of voltage-gated L-type calcium channels) stimulated release of PGF(2 alpha) in a concentration-dependent manner (P < 0.05). Thapsigargin (induces accumulation of Ca2+ in the cytoplasm by inhibiting endoplasmic reticulum Ca2+/ATPase pumps) stimulated release of PGF(2 alpha) in a concentration-dependent manner as well (P < 0.13). Oxytocin (10(-6) M), AlF4- (a. nonspecific activator of G-proteins; 10(-5) M), A23187 (10(-5) M), and melittin (a stimulator of phospholipase A(2); 10(-4) M) stimulated PGF(2 alpha) release when explants were incubated in Ca2+-free medium (P < 0.10); however, oxytocin, A23187, or melittin were unable to stimulate PGF(2 alpha) release when explants were incubated in Ca2+-free medium containing the calcium chelator EGTA (P < 0.10). This treatment did not prevent oxytocin or AlF4- from stimulating phospholipase C activity (P < 0.08). CoCl2 (a nonspecific Ca2+ channel blocker) and methoxyverapamil (a specific voltage-gated L-type Ca2+ channel blocker) prevented oxytocin from stimulating PGF(2 alpha) release (P < 0.05). Our results suggest that both extracellular and intracellular Ca2+ may be required for oxytocin to stimulate PGF(2 alpha) secretion in bovine endometrial tissue. (C) Elsevier Science Inc. 1998.