Telford N, May P C, Sinha Y N, Porter J C, Finch C E
Andrus Gerontology Center, Department of Biological Sciences, University of Southern California, Los Angeles.
Neuroendocrinology. 1992 Apr;55(4):390-5. doi: 10.1159/000126149.
DOPA was measured in the anterior pituitary and hypothalamic-hypophysial portal blood after treatment with NSD-1015, a DOPA decarboxylase inhibitor. NSD-1015 caused DOPA to accumulate in the anterior pituitary of mice and rats, and increased DOPA in the hypothalamic-hypophysial portal blood of rat. Serum prolactin was also increased. Interruption of the anterior pituitary blood supply from the hypothalamic-hypophysial system by cannulation of the entire pituitary stalk eliminated the NSD-1015-induced DOPA accumulation in the rat pituitary. We conclude that DOPA can be taken into the anterior pituitary from the portal blood of NSD-1015-treated rodents and that the anterior pituitary lacks tyrosine hydroxylase activity in both mice and rats.
在用多巴脱羧酶抑制剂NSD - 1015处理后，对垂体前叶和下丘脑 - 垂体门脉血中的多巴进行了测量。NSD - 1015使多巴在小鼠和大鼠的垂体前叶中蓄积，并使大鼠下丘脑 - 垂体门脉血中的多巴增加。血清催乳素也增加。通过插管整个垂体柄中断下丘脑 - 垂体系统对垂体前叶的血液供应，消除了NSD - 1015诱导的大鼠垂体中的多巴蓄积。我们得出结论，多巴可以从经NSD - 1015处理的啮齿动物的门脉血进入垂体前叶，并且小鼠和大鼠的垂体前叶均缺乏酪氨酸羟化酶活性。
