Lam K S, Lechan R M, Minamitani N, Segerson T P, Reichlin S
Department of Medicine, New England Medical Center, Boston, Massachusetts 02111.
Endocrinology. 1989 Feb;124(2):1077-84. doi: 10.1210/endo-124-2-1077.
Vasoactive intestinal peptide (VIP) and PRL have been reported to be colocalized in rat lactotropes. To determine whether induced hypothyroidism, known to reduce pituitary PRL concentration, also reduces pituitary concentration of VIP, rats were treated with antithyroid drugs for 3 weeks. Pituitary PRL concentration in male rats (micrograms/mg protein) was markedly reduced by this treatment (9.4 +/- 1.0 vs. 2.3 +/- 0.4 when extracted at pH 1.1, 17.9 +/- 3.0 vs. 3.4 + 0.4 when extracted at pH 7.4, 21.8 +/- 3.3 vs. 6.7 + 1.3 when extracted at pH 10.0). Contrary to expectation, pituitary VIP concentration was markedly increased in hypothyroidism; in males from 169.5 +/- 20.3 to 834.0 +/- 82.2 pg/mg protein, and in females (whose pituitary PRL had been similarly reduced) from 103.1/I +/- 34.1 to 771.6 +/- 100.9 pg/mg protein. Serum PRL was significantly reduced in hypothyroid males (7.4 +/- 1.6 vs. 28.9 +/- 12.2 ng/ml) whereas in females, serum PRL was not significantly altered (41.4 +/- 11.6 vs. 38.8 +/- 14.3 ng/ml). The effect of hypothyroidism was reversed by administration of T4 in physiological doses. The authenticity of pituitary immunoreactive VIP was further established by demonstrating chromatographic patterns by Sephadex G-50 gel exclusion and reverse phase HPLC separations identical to synthetic VIP. Immunohistochemically reactive VIP cells could not be demonstrated in normal pituitaries, but the marked increase in VIP in hypothyroid animals made it possible to visualize a population of VIP immunoreactive stellate cells which appear to be distinct from hypothyroid lactotropes and thyrotropes.
据报道,血管活性肠肽(VIP)和催乳素(PRL)在大鼠催乳细胞中共同定位。为了确定已知会降低垂体PRL浓度的诱导性甲状腺功能减退是否也会降低垂体VIP浓度,给大鼠用抗甲状腺药物治疗3周。这种治疗使雄性大鼠垂体PRL浓度(微克/毫克蛋白)显著降低(在pH 1.1提取时为9.4±1.0 vs. 2.3±0.4,在pH 7.4提取时为17.9±3.0 vs. 3.4 + 0.4,在pH 10.0提取时为21.8±3.3 vs. 6.7 + 1.3)。与预期相反,甲状腺功能减退时垂体VIP浓度显著增加;雄性从169.5±20.3增加到834.0±82.2 pg/毫克蛋白,雌性(其垂体PRL也有类似降低)从103.1/I±34.1增加到771.6±100.9 pg/毫克蛋白。甲状腺功能减退的雄性大鼠血清PRL显著降低(7.4±1.6 vs. 28.9±12.2 ng/ml),而雌性大鼠血清PRL无显著变化(41.4±11.6 vs. 38.8±14.3 ng/ml)。给予生理剂量的T4可逆转甲状腺功能减退的影响。通过葡聚糖G-50凝胶排阻色谱和反相高效液相色谱分离显示出与合成VIP相同的色谱模式,进一步证实了垂体免疫反应性VIP的真实性。在正常垂体中未发现免疫组化反应性VIP细胞,但甲状腺功能减退动物中VIP的显著增加使得可以观察到一群VIP免疫反应性星状细胞,这些细胞似乎与甲状腺功能减退的催乳细胞和促甲状腺细胞不同。