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地塞米松、地塞米松-盐、双肾单夹及自发性高血压大鼠红细胞中钠和钾离子转运加速。低钾血症和细胞体积的作用。

Sodium and potassium ion transport accelerations in erythrocytes of DOC, DOC-salt, two-kidney, one clip, and spontaneously hypertensive rats. Role of hypokalemia and cell volume.

作者信息

Duhm J, Göbel B O, Beck F X

出版信息

Hypertension. 1983 Sep-Oct;5(5):642-52. doi: 10.1161/01.hyp.5.5.642.

Abstract

Sodium (Na+) and potassium (K+) transport by the furosemide-sensitive Na+-K+ transport system, the Na+-K+ pump, and the cation leak(s) were studied in erythrocytes from DOC-water, DOC-salt, two-kidney, one clip (Sprague-Dawley), and spontaneously hypertensive rats (Wistar-Kyoto). Rubidium (Rb+) was used as a tracer for K+. After 4 weeks of DOC-salt hypertension, inward K+ (Rb+) transport by the furosemide-sensitive system was increased threefold, and the inward Na+ leak and the red cell Na+ content were elevated by about 50%. The rise in cell Na+ accelerated K+ inward and Na+ outward transport by the Na+-K4 pump, DOC-water hypertension caused similar but less pronounced changes. In two-kidney, one clip hypertension, the Na+ leak and the Na+-K+ pump rates were slightly elevated, and furosemide-sensitive Rb+ uptake tended to be increased. In spontaneously hypertensive rats, furosemide-sensitive Rb+ uptake was accelerated by 50%. The marked hypokalemia in DOC-water and DOC-salt hypertension was associated with a slight loss of red cell K+ and an increase in mean cellular hemoglobin content (MCHC), indicative of cell shrinkage. Hypokalemia induced by dietary K+ deficiency caused alterations in red cell cation transport, content, and cell volume which were qualitatively similar but more pronounced than those seen in DOC-salt hypertension. Osmotic shrinkage in vitro induced a severalfold acceleration of furosemide-sensitive Rb+ uptake, similar to that observed in rat erythrocytes shrunken in vivo in K+-deficient states. It is concluded that the acceleration of furosemide-sensitive K+ (Rb+) transport in erythrocytes of mineralocorticoid hypertensive rats is largely caused by the hypokalemia and consecutive red cell K+ loss and shrinkage, respectively. Mean cellular hemoglobin content (MCHC) is thus a parameter that must be considered in studies on Na+ and K+ transport across the membrane of rat erythrocytes.

摘要

在去氧皮质酮 - 水、去氧皮质酮 - 盐、两肾一夹(斯普拉格 - 道利大鼠)和自发性高血压大鼠(Wistar - Kyoto)的红细胞中,研究了速尿敏感的钠钾转运系统、钠钾泵以及阳离子泄漏对钠(Na⁺)和钾(K⁺)的转运情况。铷(Rb⁺)用作钾的示踪剂。去氧皮质酮 - 盐高血压4周后,速尿敏感系统的内向钾(Rb⁺)转运增加了两倍,内向钠泄漏和红细胞钠含量升高了约50%。细胞内钠的增加加速了钠钾泵介导的钾内向和钠外向转运,去氧皮质酮 - 水高血压引起了类似但不太明显的变化。在两肾一夹高血压中,钠泄漏和钠钾泵速率略有升高,速尿敏感的Rb⁺摄取趋于增加。在自发性高血压大鼠中,速尿敏感的Rb⁺摄取加速了50%。去氧皮质酮 - 水和去氧皮质酮 - 盐高血压中明显的低钾血症与红细胞钾的轻微丢失和平均细胞血红蛋白含量(MCHC)的增加有关,表明细胞收缩。饮食中钾缺乏引起的低钾血症导致红细胞阳离子转运、含量和细胞体积的改变,这些改变在性质上相似,但比去氧皮质酮 - 盐高血压中观察到的更明显。体外渗透收缩导致速尿敏感的Rb⁺摄取加速了几倍,类似于在低钾状态下体内收缩的大鼠红细胞中观察到的情况。得出的结论是,盐皮质激素性高血压大鼠红细胞中速尿敏感的钾(Rb⁺)转运加速主要分别由低钾血症以及随之而来的红细胞钾丢失和收缩引起。因此,在研究大鼠红细胞跨膜钠和钾转运时,平均细胞血红蛋白含量(MCHC)是一个必须考虑的参数。

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