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心房利钠肽调节阿米洛利敏感的钠离子跨血脑屏障转运。

Atrial natriuretic peptide modulates amiloride-sensitive Na+ transport across the blood-brain barrier.

作者信息

Ibaragi M, Niwa M, Ozaki M

机构信息

Department of Pharmacology 2, Nagasaki University School of Medicine, Japan.

出版信息

J Neurochem. 1989 Dec;53(6):1802-6. doi: 10.1111/j.1471-4159.1989.tb09246.x.

Abstract

We obtained evidence that amiloride specifically potentiates 125I-labeled alpha-rat atrial natriuretic peptide (1-28) [atrial natriuretic peptide (ANP)-(99-126); rANP] binding to cerebral capillaries isolated from the rat cerebral cortex. The binding parameters, KD of 173 pM and Bmax of 159 fmol/mg of protein, became 33 pM and 88 fmol/mg of protein, respectively, when 10(-4) M amiloride was added to the incubation medium. When the effect of rANP was investigated on in vitro 22Na+ uptake into isolated cerebral capillaries, 10(-7) M rANP significantly inhibited the uptake in the presence of 1.0 mM ouabain, 1.0 mM furosemide, and 2.0 mM LiCl in the uptake buffer, a finding suggesting a specific inhibitory effect of rANP on amiloride-sensitive Na+ transport. Thus, the possibility that ANPs control amiloride-sensitive Na+ transport at the blood-brain barrier by interacting with specific receptors has to be considered.

摘要

我们获得的证据表明,氨氯吡咪能特异性增强125I标记的α-大鼠心房利钠肽(1-28)[心房利钠肽(ANP)-(99-126);rANP]与从大鼠大脑皮层分离出的脑毛细血管的结合。当向孵育培养基中加入10^(-4) M氨氯吡咪时,结合参数解离常数(KD)为173 pM,最大结合容量(Bmax)为159 fmol/mg蛋白质,分别变为33 pM和88 fmol/mg蛋白质。当研究rANP对分离出的脑毛细血管体外22Na+摄取的影响时,在摄取缓冲液中存在1.0 mM哇巴因、1.0 mM速尿和2.0 mM LiCl的情况下,10^(-7) M rANP显著抑制了摄取,这一发现表明rANP对氨氯吡咪敏感的Na+转运具有特异性抑制作用。因此,必须考虑ANPs通过与特定受体相互作用来控制血脑屏障处氨氯吡咪敏感的Na+转运的可能性。

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