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氯化汞对大鼠垂体神经中间叶释放抗利尿激素的抑制作用。

Mercuric chloride inhibition of vasopressin release from the isolated neurointermediate lobe of the rat pituitary.

作者信息

Clifton G G, Pearce C J, Elliot K, Wallin J D

出版信息

Biochim Biophys Acta. 1986 Jul 11;887(2):189-95. doi: 10.1016/0167-4889(86)90054-6.

DOI:10.1016/0167-4889(86)90054-6
PMID:3719009
Abstract

The effects of HgCl2 and ouabain on vasopressin release and Ca2+ uptake and distribution was examined in the neurointermediate lobe of the rat pituitary. HgCl2 (0.5 mM) inhibited vasopressin release by approx. 90% in both basal and potassium depolarized states. With 0.1 mM HgCl2 vasopressin release was inhibited by 50% in the depolarized state, but release was not effected in basal state. On the other hand, ouabain (0.5 mM) caused a 3-fold stimulation of vasopressin release in the depolarized state. Both HgCl2 (0.5 mM) and ouabain (0.5 mM) increased net 45Ca+2 uptake by about 80% in groups of neurointermediate lobes. Following 45Ca+2 uptake, HgCl2 (0.5 mM), which is absorbed by the neurointermediate lobe, produced an increase in cytosolic 45Ca+2 content and a decrease in mitochondrial 45Ca+2 content compared to control. In comparison, ouabain (0.5 mM), which does not penetrate the neurointermediate lobe, gave no change in cytosolic 45Ca+2, but an increase in mitochondrial 45Ca+2. These results suggest that HgCl2 inhibits vasopressin release from the neurointermediate lobe of the rat pituitary at a point distal to Ca+2 uptake by the gland.

摘要

研究了氯化汞(HgCl2)和哇巴因对大鼠垂体神经中间叶中血管加压素释放以及钙离子摄取和分布的影响。在基础状态和钾离子去极化状态下,0.5 mM的HgCl2均可使血管加压素释放受到约90%的抑制。在去极化状态下,0.1 mM的HgCl2可使血管加压素释放受到50%的抑制,但在基础状态下释放未受影响。另一方面,在去极化状态下,0.5 mM的哇巴因可使血管加压素释放增加3倍。在神经中间叶组中,0.5 mM的HgCl2和0.5 mM的哇巴因均可使45Ca+2净摄取增加约80%。在摄取45Ca+2后,被神经中间叶吸收的0.5 mM HgCl2与对照组相比,使胞质45Ca+2含量增加,线粒体45Ca+2含量减少。相比之下,不能穿透神经中间叶的0.5 mM哇巴因对胞质45Ca+2无影响,但使线粒体45Ca+2增加。这些结果表明,HgCl2在腺体摄取Ca+2的远端位点抑制大鼠垂体神经中间叶血管加压素的释放。

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