Gonzalez Carmen, Rosas-Hernandez Hector, Jurado-Manzano Brenda, Ramirez-Lee Manuel Alejandro, Salazar-Garcia Samuel, Martinez-Cuevas Pedro Pablo, Velarde-Salcedo Aída Jimena, Morales-Loredo Humberto, Espinosa-Tanguma Ricardo, Ali Syed F, Rubio Rafael
Universidad Autónoma de San Luis Potosí, Facultad de Ciencias Químicas, San Luis Potosí 78210, México.
1] Universidad Autónoma de San Luis Potosí, Facultad de Ciencias Químicas, San Luis Potosí 78210, México [2] Neurochemistry Laboratory, Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR, USA.
Acta Pharmacol Sin. 2015 May;36(5):572-86. doi: 10.1038/aps.2014.159. Epub 2015 Apr 20.
Prolactin family hormones include growth hormone, placental lactogen and prolactin, which are able to regulate angiogenesis via NO and prostaglandins. However, their effects on vascular tone are not fully understood. The aim of this study was to evaluate the effects of prolactin family hormones on rat vascular tone in vitro.
Aortic rings were prepared from adult male rats and precontracted with phenylephrine, then treated with the hormones and drugs. The tension was measured with isometric force displacement transducer connected to a polygraph. NO production and prostacyclin release in physiological solution was determined. Cultured rat aortic endothelial cells (RAECs) were treated with the hormones and drugs, and the phosphorylation of eNOS at serine 1177 was assessed using Western bolt analysis.
Administration of growth hormone or placental lactogen (0.01-100 nmol/L) induced endothelium-dependent vasodilation. Both the hormones significantly increased the phosphorylation of eNOS in RAECs and NO level in physiological solution. Preincubation with L-NAME blocked growth hormone- or placental lactogen-induced vasodilation and NO production. Preincubation with an antibody against growth hormone receptors blocked growth hormone- and placental lactogen-induced vasodilation. Addition of a single dose of prolactin (0.01 nmol/L) induced sustained vessel relaxation, whereas multiple doses of prolactin induced a biphasic contraction-relaxation effect. The vascular effects of prolactin depended on endothelium. Prolactin significantly increased the level of prostacyclin I2 in physiological solution. Preincubation with indomethacin or an antibody against prolactin receptors blocked prolactin-induced vasodilation.
The prolactin family hormones regulate rat vascular tone, selectively promoting either relaxation or contraction of vascular smooth muscle via activation of either growth hormone receptors or prolactin receptors within the endothelium.
催乳素家族激素包括生长激素、胎盘催乳素和催乳素，它们能够通过一氧化氮（NO）和前列腺素调节血管生成。然而，它们对血管张力的影响尚未完全明确。本研究旨在评估催乳素家族激素对大鼠离体血管张力的影响。
从成年雄性大鼠制备主动脉环，用去氧肾上腺素预收缩，然后用激素和药物处理。通过连接到多道生理记录仪的等长力位移换能器测量张力。测定生理溶液中NO的产生和前列环素的释放。用激素和药物处理培养的大鼠主动脉内皮细胞（RAECs），并使用蛋白质免疫印迹分析评估内皮型一氧化氮合酶（eNOS）丝氨酸1177位点的磷酸化情况。
给予生长激素或胎盘催乳素（0.01 - 100 nmol/L）可诱导内皮依赖性血管舒张。这两种激素均显著增加RAECs中eNOS的磷酸化以及生理溶液中的NO水平。预先用L - 硝基精氨酸甲酯（L - NAME）孵育可阻断生长激素或胎盘催乳素诱导的血管舒张和NO产生。预先用抗生长激素受体抗体孵育可阻断生长激素和胎盘催乳素诱导的血管舒张。给予单剂量催乳素（0.01 nmol/L）可诱导血管持续舒张，而多剂量催乳素则诱导双相性收缩 - 舒张效应。催乳素的血管效应依赖于内皮。催乳素显著增加生理溶液中前列环素I2的水平。预先用吲哚美辛或抗催乳素受体抗体孵育可阻断催乳素诱导的血管舒张。
催乳素家族激素调节大鼠血管张力，通过激活内皮细胞内的生长激素受体或催乳素受体，选择性地促进血管平滑肌的舒张或收缩。
