URINARY KALLIKREIN - A PHYSIOLOGICAL REGULATOR OF EPITHELIAL NA+ ABSORPTION
URINARY KALLIKREIN - A PHYSIOLOGICAL REGULATOR OF EPITHELIAL NA+ ABSORPTION
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DOI：
10.1073/pnas.83.14.5345
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发表时间：
1986-07-01
影响因子：
11.1
通讯作者：
ALLES, WP
中科院分区：
文献类型：
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作者：
LEWIS, SA;ALLES, WP
哺乳动物膀胱的顶膜包含两个群体的离子电导-一个Na+选择性和阿米洛利封锁，其他阳离子选择性和阿米洛利不敏感（泄漏通道）。此外，激肽释放酶（一种酶的未知功能，通常在尿液中发现）的哺乳动物膀胱上皮细胞的粘膜溶液中导致的损失（超过2小时的时间）的阿米洛利敏感的Na+电流和泄漏电流的增加，是阿米洛利不敏感。Na+通道的水解速率是一级过程，其是浓度（活性）依赖性的，并由简单的Michaelis-Menten动力学描述，其最大速率为9.5 × 10 - 6。10-3 min-1。在人尿中测得的活性下，相应的速率常数将在24小时内使Na+通道密度降低99.5%。阿米洛利保护阿米洛利敏感的Na+通道免于降解，但不保护泄漏途径。泄漏途径的水解速率以及水解动力学与Na+通道所述相同。感兴趣的是，泄漏途径被水解成似乎在顶膜和粘膜溶液之间分配的形式（不稳定的泄漏途径）。这些结果和以前的研究结果表明，激肽释放酶在盐和水bomeostasis的调节作用。
The apical membrane of the mammalian urinary bladder contains two populations of ionic conductances-one Na+ selective and amiloride blockade, the other cation selective and amiloride insensitive (a leak channel). Addition of kallikrein (an enzyme of unknown function normally found in urine) to the mucosal solution of the mammalian urinary bladder epithelium resulted in the loss (over a 2-hr period) of amiloride-sensitive Na+ current and an increase in the leak current that is amiloride insensitive. The rate of hydrolysis of Na+ channels is a first-order process that is concentration (activity) dependent and described by simple Michaelis-Menten kinetics with a maximum rate of 9.5 .times. 10-3 min-1. At the activities measured in human urine, the corresponding rate constant will decrease Na+ channel density by 99.5% in 24 hr. Amiloride protects the amiloride-sensitive Na+ channels from degradation but not the leak pathway. The rate of hydrolysis of the leak pathway as well as the kinetics of hydrolysis are the same as that described for the Na+ channel. Of interest is that the leak pathway is hydrolyzed into a form that seems to partition between the apical membrane and mucosal solution (an unstable leak pathway). These results and previous findings suggest a regulatory role for kallikrein in salt and water bomeostasis.