Renal synthesis and urinary excretion of eicosanoids during pregnancy in rats.

Renal synthesis and urinary excretion of eicosanoids during pregnancy in rats.
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DOI:
10.1152/ajprenal.1987.253.6.f1197
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发表时间:
1987-12
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Kirk P. Conrad;Michael J. Dunn
Kirk P. Conrad;Michael J. Dunn
中科院分区:
其他
文献类型:
--
作者:
Kirk P. Conrad;Michael J. Dunn

文献摘要

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我们通过评估体外肾组织中前列腺素的产生来测试血管扩张性前列腺素(PGs)是否介导了母体肾脏循环对妊娠的适应性。我们推断,如果前列腺素是至关重要的,那么这些激素的局部合成速度很可能会增加。妊娠6天、12天和20天的大鼠肾小球中,前列腺素F2α、前列腺素E_2或6-酮-前列腺素F1α的基础合成或刺激合成均不比处女对照组大。妊娠大鼠肾皮质切片产生的前列腺素E_2和6-酮-前列腺素F_1α也不比处女大鼠多。PGE2和6-keto-PGF1α的24小时尿排泄率在妊娠期间显著增加(均P<0.05),但PGF2α的排泄率无明显变化。在妊娠中期,当尿中PGE2和6-keto-PGF1α的排泄量最大时,这些PGs的髓质合成在处女和妊娠动物中被发现是相似的。这项研究没有显示妊娠大鼠肾组织合成PGs的增加,这与我们之前的研究是一致的,在该研究中,抑制环氧合酶并没有减少妊娠期肾脏血流动力学的增加,也没有恢复对外源性血管紧张素II减弱的肾脏升压反应。综上所述,我们得出结论,在大鼠中,PGs很可能不参与妊娠期间观察到的肾脏循环的变化。
We tested whether vasodilatory prostaglandins (PGs) mediate the adaptation of the maternal renal circulation to pregnancy by assessing production of PGs by kidney tissues in vitro. We reasoned that if PGs are crucial, then local synthetic rates of these hormones would most likely be increased. Glomeruli harvested from gravid rats of gestational days 6, 12, and 20 did not demonstrate greater basal or stimulated syntheses of PGF2 alpha, PGE2, or 6-keto-PGF1 alpha than those from virgin controls. Production of PGE2 and 6-keto-PGF1 alpha by renal cortical slices obtained from pregnant rats was not greater than that of virgins either. Urine 24-h excretory rates of PGE2 and 6-keto-PGF1 alpha, but not PGF2 alpha, were significantly increased during pregnancy (all P less than 0.05 from prepregnant levels). During midgestation, when urinary excretion of PGE2 and 6-keto-PGF1 alpha was greatest, medullary syntheses of these PGs were found to be comparable between virgin and gravid animals. The present study, which fails to show augmented synthesis of PGs by renal tissues derived from gravid rats, is consistent with our previous investigation in which cyclooxygenase inhibition did not reduce the gestational increase of renal hemodynamics or restore the attenuated renal pressor responsiveness to exogenous angiotensin II. Taken together, we conclude that in rats, PGs most likely do not mediate the alterations in the renal circulation observed during pregnancy.