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急性肾衰竭大鼠肾刷状缘膜中对氨基马尿酸、四乙铵和D-葡萄糖的转运

Transport of p-aminohippurate, tetraethylammonium and D-glucose in renal brush border membranes from rats with acute renal failure.

作者信息

Hori R, Takano M, Okano T, Inui K

出版信息

J Pharmacol Exp Ther. 1985 Jun;233(3):776-81.

PMID:2989496
Abstract

Transport of D-glucose, p-aminohippurate and tetraethylammonium has been studied using renal brush border membrane vesicles isolated from rats with uranyl nitrate-induced acute renal failure (ARF). Initial rate and overshoot magnitude of Na+ gradient-dependent D-glucose uptake were decreased in brush border membrane vesicles from ARF rats compared with normal rats, although there was no significant difference on D-glucose uptake in the presence of equilibrated Na+ between normal and ARF rats. Uptake of p-aminohippurate by membrane vesicles from ARF rats did not differ from normal membrane vesicles. Uptake of tetraethylammonium with or without an H+ gradient was decreased in membrane vesicles from ARF rats compared with normal rats. Dissipation rate of H+ gradient across brush border membranes did not differ between both groups. In vitro incubation of normal brush border membrane vesicles with uranyl nitrate caused no alteration in any substrate transport. However, enzyme activities such as (Na+ + K+)-adenosine triphosphatase in renal cortical homogenate were inhibited markedly in the presence of uranyl nitrate. These results suggest that uranyl nitrate-induced ARF caused alterations in the transport properties of renal brush border membranes and that these transport dysfunctions were not due to the direct effect of uranyl nitrate, but could be secondarily induced after the impairment of the integrity for tubular cells.

摘要

利用从硝酸铀酰诱导的急性肾衰竭(ARF)大鼠分离的肾刷状缘膜囊泡,研究了D-葡萄糖、对氨基马尿酸盐和四乙铵的转运。与正常大鼠相比,ARF大鼠刷状缘膜囊泡中Na⁺梯度依赖性D-葡萄糖摄取的初始速率和超调幅度降低,尽管在正常大鼠和ARF大鼠中,在平衡Na⁺存在下D-葡萄糖摄取没有显著差异。ARF大鼠膜囊泡对对氨基马尿酸盐的摄取与正常膜囊泡没有差异。与正常大鼠相比,ARF大鼠膜囊泡中有无H⁺梯度时四乙铵的摄取均降低。两组之间刷状缘膜上H⁺梯度的消散速率没有差异。用硝酸铀酰对正常刷状缘膜囊泡进行体外孵育,未引起任何底物转运的改变。然而,在硝酸铀酰存在下,肾皮质匀浆中的酶活性如(Na⁺+K⁺)-三磷酸腺苷酶被显著抑制。这些结果表明,硝酸铀酰诱导的ARF导致肾刷状缘膜转运特性的改变,并且这些转运功能障碍不是由于硝酸铀酰的直接作用,而是可能在肾小管细胞完整性受损后继发诱导产生的。

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