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頁籤選單縮合
題名 | K[90a7] Secretion and Luminal Flow in Distal Nephron=遠端腎元腎小管腔內流量與鉀離子分泌之關係 |
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作者 | Taniguchi, Junichi; |
期刊 | 臺灣腎臟醫學會雜誌 |
出版日期 | 20080900 |
卷期 | 22:3 2008.09[民97.09] |
頁次 | 頁143-158 |
分類號 | 415.74 |
語文 | eng |
關鍵詞 | 腎; 鉀離子; K[90a7] excretion; Distal K[90a7] secretion; Flow-dependence; Maxi K[90a7] channel; ROMK channel; |
英文摘要 | Mammalian kidney regulates urinary K(superscript +) excretion to maintain extracellular K(superscript +) concentration constant by controlling K(superscript +) secretion from distal nephron. In addition to hormonal regulation, the distal K(superscript +) secretion depends on luminal flow. This flow-dependent K(superscript +) secretion is the reason of diuretic-induced hypokalemia. ROMK and maxi K(superscript +) channels were found in the luminal membrane of distal nephron. Because mineralocorticoid stimulated ROMK channel synthesis, they had been thought as K(superscript +) secretory pathway of luminal membrane in distal nephron. However, investigations for recent about 10 years have disclosed the role of maxi K(superscript +) channels as the pathway of flow-dependent K(superscript +) secretion, Flow-induced mechanical stress of luminal membrane activates the maxi K(superscript +) channels by increasing Ca(superscript 2+) entry via stretch-activated cation channels. The flow-dependent K(superscript +) secretion was lost in cortical collecting duct (CCD) isolated from the knockout mice lacking transient receptor potential vaniloid 4 channels that were stretch-activated and cation permeable. A selective blocking of maxi K(superscript +) channel inhibited the flow-dependent component oft secretion but not the flow-independent component in rabbit CCD. Kaliuretic response disappeared in either knockout mouse lacking α or β1 subunit of maxi K(superscript +) channel. Either disrupting ROMK channel gene or applying iberiotoxin, a maxi K(superscript +) channel blocker, reduced urinary K(superscript +) excretion by 50%, respectively, which suggests equal contribution of maxi K(superscript +) channels and ROMK channels to the distal K(superscript +) secretion in normal condition. Hyperkalemia causes diuresis by suppressing isotonic reabsorption in proximal tubule. Thus, the flow-dependent K(superscript +) secretion via maxi K(superscript +) channels may correct the hyperkalemia instantaneously, whereas hormonal regulation of ROMK channels may correct it chronically. |
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