遗传性下丘脑性尿崩症的布拉德福德大鼠的肾脏前列腺素激肽释放酶-激肽系统
The renal prostaglandin kallikrein-kinin-system in Brattleboro rats with hereditary hypothalamic diabetes insipidus.
作者信息
Somova L, Ivanova M, Zaharieva S
出版信息
Acta Physiol Pharmacol Bulg. 1985;11(4):69-73.
The results of estimation of renal prostaglandin (PG) excretion showed a significantly decreased excretion of PGE2 by 71% and that of PGF2 alpha--by 28% in rats with hereditary diabetes insipidus (DI), compared to the control Long Evans (LE) rats. The results suggested an inhibition of renal PG synthesis in DI rats due to the absence of stimulatory effect of ADN in DI rats lacking ADH. An inverse correlation between plasma renin activity and renal PG excretion was found (r = --0.36). The renal kallikrein excretion of DI rats was not significantly different compared to that of LE rats. An attempt for explanation of these results was made.
遗传性尿崩症（DI）大鼠肾前列腺素（PG）排泄的估计结果显示，与对照长 Evans（LE）大鼠相比，PGE2 的排泄显著减少了 71%，PGF2α 的排泄减少了 28%。结果表明，在缺乏抗利尿激素（ADH）的 DI 大鼠中，由于不存在抗利尿激素（ADN）的刺激作用，肾 PG 合成受到抑制。发现血浆肾素活性与肾 PG 排泄之间呈负相关（r = -0.36）。DI 大鼠的肾激肽释放酶排泄与 LE 大鼠相比无显著差异。对这些结果进行了解释。
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