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前列腺素E2在调节蛙膀胱低渗和高渗透水性中的作用

Role of prostaglandin E2 in regulation of low and high water osmotic permeability in frog urinary bladder.

作者信息

Parnova R G, Schakhmatova E I, Plesneva S A, Getmanova E V, Korolev E V, Komissarchik Y Y, Natochin Y V

机构信息

Sechenov Institute of Evolutionary Physiology and Biochemistry, Saint Petersburg, Russia.

出版信息

Biochim Biophys Acta. 1997 Apr 24;1356(2):160-70. doi: 10.1016/s0167-4889(96)00175-9.

DOI:10.1016/s0167-4889(96)00175-9
PMID:9150274
Abstract

The water osmotic permeability of frog urinary bladder was found to be increased from 0.08 +/- 0.01 to 1.28 +/- 0.20 microl/min cm2 when serosal bathing medium was changed 4 times for a fresh Ringer solution. High epithelium permeability is accompanied by an increased content of cyclic AMP in the bladder tissue (by 42%, P < 0.01), higher activity of both basal and forskolin-stimulated membrane adenylate cyclase (AC) (by 109% and 74%, respectively, P < 0.05) and by appearance of aggregates of intramembranous particles in the apical membrane. The water flow was inhibited by 10(-9)-10(-5) M prostaglandin E2 (PGE2); the inhibitory effect was eliminated in the presence of 10(-4) M N-ethylmaleimide. The increase of water permeability due to changes of the bathing medium was accompanied by a decrease of serosal PGE2 concentration from 14.8 +/- 1.0 in the 1st solution to 0.6 +/- 0.1 nM in the 5th. 10(-6) M PGE2 in vitro inhibited the activity of membrane AC from highly permeable bladders by 33.4% (P < 0.02). Pretreatment of the membranes with 10 microg/ml pertussis toxin (PT) completely reversed this effect (+149%, P < 0.01). A significant activation of AC was also observed under 10(-10) M PGE2 (by 196%). These data demonstrate that the water permeability could be markedly increased independently of ADH, suggesting that the trigger role in activation of water transport is played by a decreased level of PGE2 which could stimulate AC.

摘要

当将浆膜浴液更换4次为新鲜的林格液时,发现青蛙膀胱的水渗透通透性从0.08±0.01增加到1.28±0.20微升/分钟·平方厘米。高上皮通透性伴随着膀胱组织中环磷酸腺苷含量的增加(增加42%,P<0.01)、基础和福斯高林刺激的膜腺苷酸环化酶(AC)活性的升高(分别增加109%和74%,P<0.05)以及顶端膜中膜内颗粒聚集体的出现。水流量受到10^(-9)-10^(-5)M前列腺素E2(PGE2)的抑制;在存在10^(-4)M N-乙基马来酰亚胺的情况下,抑制作用消除。由于浴液变化导致的水通透性增加伴随着浆膜PGE2浓度从第一种溶液中的14.8±1.0降至第五种溶液中的0.6±0.1纳摩尔。10^(-6)M PGE2在体外抑制高通透性膀胱膜AC的活性33.4%(P<0.02)。用10微克/毫升百日咳毒素(PT)预处理膜完全逆转了这种作用(增加149%,P<0.01)。在10^(-10)M PGE2下也观察到AC的显著激活(增加196%)。这些数据表明,水通透性可独立于抗利尿激素而显著增加,提示PGE2水平降低可能在激活水转运中起触发作用,其可刺激AC。

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