Cation transport goes with the flow.
Cation transport goes with the flow.
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阳离子传输随流而行。
DOI：
10.1152/ajprenal.00331.2012
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Carattino,MarceloD
中科院分区：
文献类型：
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作者：
Carattino,MarceloD
皮质部集合管的钠重吸收和钾分泌受到管腔液体流动的严格调节24(9，11)。提高离体管的灌注率会对上皮的顶端表面施加两种力，即流体剪应力和周向拉伸。Flores et.艾尔最新一期的《美国生理学-肾脏生理学》提供了令人信服的27项证据，证明流体剪切力通过激活胞浆磷脂酶A2(CPLA2)增加前列腺素E2 28(PGE2)的产生和释放。这项研究揭示了一种新的机制，即环氧合酶衍生的前列腺素可以不同地调节收集管中钠和钾的运输，以响应流体动力的变化。31尿钠、钾最终排出量在末梢32曲管和连接小管及皮质集合管中调节。盐皮质激素33-醛固酮作用于肾单位的这一区域，促进钠和水的重吸收，从而增加血容量，从而增加动脉血压。上皮性钠通道35(ENaC)构成了36收集管主细胞钠重吸收的限速步骤。在这些细胞的顶端37膜上发现了两个钾传导通道，即肾外髓质钾通道(ROMK)和大电导钙激活钾通道(BK)。ROMK通道介导基线39钾的分泌，而BK通道在流刺激的钾40分泌中起主要作用。提高管腔流速可增加ENaC介导的钠重吸收和BK-41介导的钾分泌(9，11)。由于阻断ENaC活性阻止了流动刺激的42钾的分泌，有人认为ENaC介导的钠重吸收提供了钾分泌所需的43个有利的电化学梯度。44
Sodium reabsorption and potassium secretion in the cortical collecting duct are tightly regulated 24 by luminal fluid flow (9, 11). Raising perfusion rates in isolated tubules exerts two forces on the 25 apical surface of the epithelium, fluid shear stress and circumferential stretch. Flores et. al. in 26 the current issue of the American Journal of Physiology–Renal Physiology provide compelling 27 evidence that fluid shear stress increases the production and release of prostaglandin E2 28 (PGE2) through activation of cytosolic phospholipase A2 (cPLA2). This study discloses a novel 29 mechanism whereby cyclooxygenase-derived prostanoids differentially regulate sodium and 30 potassium transport in the collecting duct in response to changes in hydrodynamic forces. 31The final amount of sodium and potassium eliminated in the urine is adjusted in the late distal 32 convoluted and connecting tubules and cortical collecting ducts. The mineralocorticoid 33 aldosterone acts in this region of the nephron promoting sodium and water reabsorption, 34 increasing blood volume and, therefore arterial blood pressure. The epithelial sodium channel 35 (ENaC) constitutes the rate-limiting step for sodium reabsorption in principal cells of the 36 collecting duct. Two potassium conductive channels have been identified in the apical 37 membrane of these cells, the renal outer medullary potassium (ROMK) channel and the large-38 conductance Ca2+-activated potassium (BK) channel (8). ROMK channels mediate baseline 39 potassium secretion, while BK channels play a major role in flow-stimulated potassium 40 secretion. Raising luminal flow rates increases ENaC-mediated sodium reabsorption and BK-41 mediated potassium secretion (9, 11). Since blocking ENaC activity prevents flow-stimulated 42 potassium secretion, it was proposed that ENaC-mediated sodium reabsorption provides the 43 favorable electrochemical gradient required for potassium secretion. 44