Prolactin directly stimulates transcellular active calcium transport in the duodenum of female rats
Prolactin directly stimulates transcellular active calcium transport in the duodenum of female rats
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DOI：
10.1139/cjpp-79-5-430
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发表时间：
2001-05-01
影响因子：
2.1
通讯作者：
Krishnamra, N
中科院分区：
文献类型：
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作者：
Charoenphandhu, N;Limlomwongse, L;Krishnamra, N
催乳素被认为是妊娠期和哺乳期的一种新型钙调节激素。在几种实验模型中，它刺激被动和主动十二指肠钙转运。我们的研究是在性成熟的雌性Wistar大鼠（200-250 g）上进行的，以研究催乳素对十二指肠中钙转运的直接作用。为了评估催乳素对十二指肠总钙转运的影响，我们给大鼠腹腔注射0.4、0.6和0.8 mg/kg催乳素。总钙转运分为电压依赖性，溶剂拖曳诱导，和跨细胞的主动通量施加短路电流和粘膜葡萄糖置换甘露醇。分别研究催乳素对每个通量的影响。最后，为了评估催乳素对十二指肠跨细胞活性通量的直接作用，我们将十二指肠段直接暴露于已加入到serovir溶液中的催乳素（含或不含钙转运抑制剂）。我们发现，0.6和0.8 mg/kg催乳素ip显著增加了总粘膜-浆膜钙流，从对照值（nmol. hr（-1）.cm（-2））分别为34.53 +/- 6.81至68.07 +/- 13.53（P < 0.05）和84.43 +/- 19.72（P < 0.01）。催乳素还能增强溶剂阻力诱导的钙流和跨细胞活性钙流，但对电压依赖性钙流无明显影响。直接暴露于200、400和800 ng/mL催乳素的十二指肠节段显示跨细胞活性钙吸收以剂量依赖性方式显著增加，即，从对照值（nmol.hr（-1）.cm（-2））2.94 +/- 0.47分别降至5.45 +/- 0.97（P < 0.01）、8.09 +/- 0.52（P < 0.001）和18.42 +/- 2.92（P < 0.001）。其直接作用被粘膜暴露于50 μ M氯化镧（一种钙转运蛋白竞争剂）和serovine暴露于0.1 mM三氟拉嗪（一种Ca 2 +-ATP酶抑制剂）所抑制。这些研究表明，十二指肠是催乳素的靶器官，催乳素增强跨细胞主动钙转运。
Prolactin has been postulated to be a novel calcium-regulating hormone during pregnancy and lactation. It stimulates both passive and active duodenal calcium transport in several experimental models. Our study was performed on sexually mature female Wistar rats (200-250 g) to study the direct action of prolactin on calcium transport in the duodenum using the Ussing chamber technique. To evaluate the effect of prolactin on total calcium transport in the duodenum, we intraperitoneally injected rats with 0.4, 0.6, and 0.8 mg/kg prolactin. The total calcium transport was divided into voltage-dependent, solvent drag-induced, and transcellular active fluxes by applying short-circuit current and by mucosal glucose replacement with mannitol. The effect of prolactin on each flux was studied separately. Finally, to evaluate the direct action of prolactin on duodenal transcellular active flux, we directly exposed duodenal segments to prolactin that had been added to the serosal solution with or without calcium transport inhibitors. We found that 0.6 and 0.8 mg/kg prolactin ip significantly increased the total mucosa-to-serosa calcium flux from the control value (nmol.hr(-1).cm(-2)) of 34.53 +/- 6.81 to 68.07 +/- 13.53 (P < 0.05) and 84.43 +/- 19.72 (P < 0.01), respectively. Prolactin also enhanced the solvent drag-induced calcium flux and transcellular active calcium flux, but not the voltage-dependent calcium flux. The duodenal segments directly exposed to 200, 400, and 800 ng/mL prolactin showed a significant increase in the transcellular active calcium absorption in a dose-dependent manner, i.e., from the control value (nmol.hr(-1).cm(-2)) of 2.94 +/- 0.47 to 5.45 +/- 0.97 (P < 0.01), 8.09 +/- 0.52 (P < 0.001), and 18.42 +/- 2.92 (P < 0.001), respectively. Its direct action was inhibited by mucosal exposure to 50 muM lanthanum chloride, a calcium transporter protein competitor, and serosal exposure to 0.1 mM trifluoperazine, a Ca2+-ATPase inhibitor. These studies demonstrate that the duodenum is a target organ of prolactin, which enhances transcellular active calcium transport.