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大鼠结肠顶端膜囊泡中钠氢交换的特性研究

Characterization of Na-H exchange in apical membrane vesicles of rat colon.

作者信息

Rajendran V M, Binder H J

机构信息

Department of Internal Medicine, Yale University, New Haven, Connecticut 06510.

出版信息

J Biol Chem. 1990 May 25;265(15):8408-14.

PMID:2160456
Abstract

This study establishes the characteristics of electroneutral Na-H exchange present in apical membrane vesicles isolated from colonocytes of rat large intestine. An outward directed proton gradient stimulated 22Na uptake and demonstrated transient accumulation that was not altered by voltage clamping with K and its ionophore, valinomycin. Amiloride inhibited proton gradient-stimulated 22Na (0.1 mM) uptake by 97% by a noncompetitive mechanism with a Ki of 27 microM. 5-(N-ethyl-N-isopropyl)amiloride, an amiloride analogue which is a specific potent inhibitor of electroneutral Na-H exchange, inhibited proton gradient-stimulated 22Na uptake with a Ki of 400 nM. Increasing Na concentration saturated the proton gradient-stimulated 22Na uptake with an apparent Km of 11.7 +/- 2.2 mM. Increasing intravesicular proton concentration also resulted in saturation of 22Na uptake with a Km of 2.8 microM. Proton gradient-stimulated 22Na uptake was inhibited significantly by 10 mM Na+, Li+, and NH4+, while outward directed gradients of these ions in the absence of proton gradient accelerated 22Na uptake. The mechanism of Li+ inhibition of proton gradient-stimulated 22Na uptake was competitive with a Ki of 2 mM. 22Na uptake either stimulated by an outward directed Na gradient (i.e. Na-Na exchange) at pH 5.5, 6.5, and 7.5 or stimulated by 10-fold outward directed proton gradient at different pH values was similar; observations that do not suggest proton activation of Na-H exchange. We conclude from these results that proton gradient-stimulated 22Na uptake in colonic apical membrane vesicles represents tightly coupled electro-neutral Na-H exchange with several kinetic properties unlike those described in other epithelia.

摘要

本研究确定了从大鼠大肠结肠细胞分离的顶端膜囊泡中存在的电中性钠氢交换的特征。外向质子梯度刺激了22Na摄取,并显示出瞬时积累,这种积累不会因用钾及其离子载体缬氨霉素进行电压钳制而改变。氨氯吡脒通过非竞争性机制抑制质子梯度刺激的22Na(0.1 mM)摄取,抑制率达97%,其抑制常数Ki为27 microM。5-(N-乙基-N-异丙基)氨氯吡脒是氨氯吡脒的类似物,是电中性钠氢交换的特异性强效抑制剂,抑制质子梯度刺激的22Na摄取,其Ki为400 nM。增加钠浓度使质子梯度刺激的22Na摄取达到饱和,表观Km为11.7±2.2 mM。增加囊泡内质子浓度也导致22Na摄取饱和,Km为2.8 microM。质子梯度刺激的22Na摄取受到10 mM Na+、Li+和NH4+的显著抑制,而在没有质子梯度的情况下,这些离子的外向梯度会加速22Na摄取。Li+抑制质子梯度刺激的22Na摄取的机制具有竞争性,Ki为2 mM。在pH 5.5、6.5和7.5时,由外向钠梯度(即钠-钠交换)刺激的22Na摄取或在不同pH值下由10倍外向质子梯度刺激的22Na摄取是相似的;这些观察结果并不表明质子对钠氢交换有激活作用。从这些结果我们得出结论,结肠顶端膜囊泡中质子梯度刺激的22Na摄取代表紧密偶联的电中性钠氢交换,其具有一些不同于其他上皮细胞中描述的动力学特性。

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