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硫脲对血管升压素刺激的尿素跨蟾蜍膀胱转运的抑制作用。

Inhibition of vasopressin-stimulated urea transport across the toad bladder by thiourea.

作者信息

Eggena P

出版信息

J Clin Invest. 1973 Nov;52(11):2963-70. doi: 10.1172/JCI107493.

Abstract

The mammalian antidiuretic hormone, 8-arginine-vasopressin, was found to increase net mucosal-to-serosal urea flux across the isolated toad urinary bladder 13-fold. This urea flux was accompanied by a 24-fold increase in solute-linked water movement across the membrane. Net urea flux and urea-linked volume flux were inhibited by 50% or more when thiourea was added to the mucosal medium at concentrations equal to those of urea. In contrast, thiourea did not inhibit osmotic water flux across the bladder in the presence of vasopressin. These observations are consistant with the view that thiourea and urea compete for a common site on a membrane carrier molecule. When bladders were exposed to vasopressin on the serosa and subsequently fixed with 1% glutaraldehyde on the mucosa, they were found to retain 74% of their prefixation permeability to urea. Net urea flux across these fixed bladders (in the absence of vasopressin) was markedly inhibited by thiourea, whereas osmotic water flux was not inhibited. These studies suggest that vasopressin induces the formation of "urea-channels" in the membrane that can be preserved by glutaraldehyde and blocked by thiourea.

摘要

已发现哺乳动物抗利尿激素8 - 精氨酸加压素可使分离的蟾蜍膀胱黏膜至浆膜的尿素净通量增加13倍。这种尿素通量伴随着溶质相关水跨膜移动增加24倍。当以与尿素浓度相同的浓度将硫脲添加到黏膜介质中时,尿素净通量和尿素相关体积通量被抑制50%或更多。相比之下,在存在加压素的情况下,硫脲并不抑制跨膀胱的渗透水通量。这些观察结果与硫脲和尿素竞争膜载体分子上的共同位点这一观点一致。当膀胱在浆膜侧暴露于加压素,随后在黏膜侧用1%戊二醛固定时,发现它们对尿素的固定前通透性保留了74%。硫脲显著抑制了这些固定膀胱(在无加压素的情况下)的尿素净通量,而渗透水通量未受抑制。这些研究表明,加压素可诱导膜中形成“尿素通道”,该通道可被戊二醛保存并被硫脲阻断。

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