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本工作探讨VIP在下丘脑水平对PRL和β-EP释放的调节,结果表明,所用三种剂量的VIP均显著兴奋PRL的释放,兴奋效应与VIP剂量相关;各剂量VIP对β-EP的释放均无明显影响,提示VIP可经某种下丘脑机制兴奋PRL的释放。我们的结果还进一步证明,VIP兴奋PRL的释放似与抑制DA的作用无关。另外,应用体外培养的正常大鼠前叶垂体细胞,观察10~(-10)～10~(-6)mol/L的VIP对PRL和β-EP释放的影响及其与细胞外Ca~(2+)浓度的关系,看到VIP可直接兴奋垂体细胞释放PRL,且具剂量相关效应;VIP兴奋PRL的释放与胞外Ca~(2+)浓度无关。剂量达10~(-7)mol/L的VIP仍不影响垂体细胞β-EP的释放。另用新鲜制备的正常大鼠离散前叶垂体细胞,比较VIP对细胞内cAMP和胞内Ca~(2+)的影响,结果表明,10~(-7)mol/L的VIP显著升高细胞内Ca~(2+)浓度,也显著升高胞内cAMP的水平,但后者可被2.0mmol/L EGTA消除,说明胞内cAMP水平的改变有赖于胞外Ca~(2+)的存在,联想上述VIP兴奋PRL的释放却与胞外Ca~(2+)的存在与否无关,提示VIP兴奋PRL的释放似由胞内Ca~(2+)而非cAMP介导信息跨膜传递。
This study investigated the regulation of VIP on hypothalamic levels of PRL and β-EP release. The results showed that the three doses of VIP were significantly excited PRL release, the excitement effect and VIP dose; VIP at each dose of β-EP release No significant effect, suggesting VIP can be excited by some kind of hypothalamic PRL release. Our results further demonstrate that VIP-stimulated release of PRL appears to be independent of the role of DA suppression. In addition, the effect of VIP of 10 ~ (-10) ~ 10 ~ (-6) mol / L on the release of PRL and β-EP and the relationship with extracellular Ca ~ (superscript +) 2+), we found that VIP could directly excite pituitary cells to release PRL with a dose-dependent effect. The release of VIP-excited PRL was not related to the concentration of extracellular Ca 2+. VIP doses up to 10 -7 mol / L did not affect the release of β-EP in pituitary cells. Another freshly prepared normal rat anterior lobe of isolated anterior pituitary cells, VIP compared intracellular cAMP and intracellular Ca ~ (2+), the results showed that 10 ~ (-7) mol / L of VIP significantly increased cells Intracellular Ca 2+ concentration also significantly increased the level of intracellular cAMP, but the latter could be eliminated by 2.0 mmol / L EGTA, indicating that intracellular cAMP level changes depend on the presence of extracellular Ca 2+ , Suggesting that the release of PRL in association with VIP was not related to the presence or absence of extracellular Ca ~ (2+), suggesting that the release of VIP might appear to be mediated by intracellular Ca ~ (2+) rather than cAMP.