Whiteaker S S, Mirando M A, Becker W C, Peters D N
Department of Animal Sciences, Washington State University, Pullman 99164-6332, USA.
Domest Anim Endocrinol. 1995 Jan;12(1):95-104. doi: 10.1016/0739-7240(94)00012-p.
The mechanism for the luteolytic release of prostaglandin (PG)F2 alpha in swine is not known. This study examined the potential role of oxytocin (OT)-induced phosphoinositide (PI) hydrolysis in promoting PGF2 alpha secretion in vitro from the endometrium of cyclic gilts on Day 15 postestrus. In Experiment 1, endometrial PI hydrolysis was increased (P < 0.05) by 100 nM OT and was increased quadratically (P < 0.05) by LiCl, but was not affected by the LiCl x OT interaction (P > 0.30). PI hydrolysis was maximal at 50 mM LiCl and declined at 100 mM LiCl. In Experiment 2, endometrial PI hydrolysis and PGF2 alpha secretion were similarly increased (P < 0.01) by 0, 0.1, 1, 10, and 100 nM OT in a dose-dependent manner. In Experiment 3, the linear increase in PI hydrolysis occurring 0, 3, 5, 10, and 20 min after treatment was greater (P = 0.01) for tissue treated with 100 nM OT than for the tissue treated with 0 nM OT. The quadratic increase (P < 0.05) in PGF2 alpha secretion occurring 0, 3, 5, 10, and 20 min after treatment was greater (P < 0.05) for tissue treated with 100 nM OT than for the tissue treated with 0 nM OT. In Experiment 4, AlF4- (an activator of Gp and phospholipase C) similarly increased (P < 0.01) PI hydrolysis and PGF2 alpha secretion. In Experiment 5, PI hydrolysis (P < 0.01) and PGF2 alpha secretion (P < 0.05) were increased by 100 nM OT but were not stimulated by cholera toxin (an activator of Gs and adenylate cyclase). Cholera toxin also did not enhance PI hydrolysis and PGF2 alpha secretion in response to 0.1 or 100 nM OT. These results are consistent with the hypothesis that OT may induce PI hydrolysis to stimulate the endometrial secretion of PGF2 alpha during corpus luteum regression in swine.
猪体内前列腺素（PG）F2α的黄体溶解释放机制尚不清楚。本研究探讨了催产素（OT）诱导的磷酸肌醇（PI）水解在促进发情后第15天发情周期母猪子宫内膜体外分泌PGF2α中的潜在作用。在实验1中，100 nM OT使子宫内膜PI水解增加（P < 0.05），LiCl使其呈二次方增加（P < 0.05），但不受LiCl×OT相互作用的影响（P > 0.30）。PI水解在50 mM LiCl时最大，在100 mM LiCl时下降。在实验2中，0、0.1、1、10和100 nM OT以剂量依赖方式使子宫内膜PI水解和PGF2α分泌同样增加（P < 0.01）。在实验3中，处理后0、3、5、10和20分钟时，100 nM OT处理的组织PI水解的线性增加幅度大于（P = 0.01）0 nM OT处理的组织。处理后0、3、5、10和20分钟时，100 nM OT处理的组织PGF2α分泌的二次方增加幅度大于（P < 0.05）0 nM OT处理的组织。在实验4中，AlF4-（Gp和磷脂酶C的激活剂）同样增加（P < 0.01）PI水解和PGF2α分泌。在实验5中，100 nM OT使PI水解增加（P < 0.01），PGF2α分泌增加（P < 0.05），但霍乱毒素（Gs和腺苷酸环化酶的激活剂）未刺激其增加。霍乱毒素也未增强0.1或100 nM OT刺激后的PI水解和PGF2α分泌。这些结果与以下假设一致：在猪黄体退化过程中，OT可能诱导PI水解以刺激子宫内膜分泌PGF2α。
