Properties of an inwardly rectifying ATP-sensitive K+ channel in the basolateral membrane of renal proximal tubule.
Properties of an inwardly rectifying ATP-sensitive K+ channel in the basolateral membrane of renal proximal tubule.
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肾近曲小管基底外侧膜内向整流 ATP 敏感 K 通道的特性。
DOI：
10.1085/jgp.111.1.139
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Segal,AS
中科院分区：
文献类型：
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作者：
Mauerer,UR;Boulpaep,EL;Segal,AS
*耶鲁大学医学院细胞与分子生理学系，康涅狄格州纽黑文06520；近端小管细胞基底外侧膜（BLM）的钾电导是运输的关键调节因子，因为它是负细胞膜电位的主要决定因素，并且是Na， K - atp酶泵的泵漏耦合所必需的。尽管具有这种关键的生理作用，但这种电导的特性尚未完全表征，部分原因是难以获得BLM。我们已经研究了解离的，极化的Ambystoma近端小管细胞中这种blmk电导的特性。几乎所有在Ambystoma细胞上形成的密封都包含向内整流的K通道（斜率，在24.5 0.6 pS内，弦向外3.7 0.4 pS）。这种整流部分是由内部的Mg2介导的。通道的打开概率随着超极化的增加而适度增加。向内导电性能用饱和结合-非结合模型来描述。该通道导电Tl和K，但对Na， Rb, Cs, Li， NH4或Cl没有显著的电导。该通道被钡和磺脲类药物格列本脲抑制，但不被四乙基铵抑制。通道衰竭通常发生在没有ATP的情况下，但细胞质中添加0.2 mM ATP（或任何可水解的三磷酸核苷）可以无限期地维持通道活性。磷酸化过程本身不能维持通道活性。高剂量的ATP（或其他三磷酸核苷）可逆地抑制该通道。K通道开启剂二氮氧化物在0.2 mM ATP存在下打开通道，但不减轻毫摩尔剂量ATP的抑制作用。我们得出结论，这个K通道是近端小管中主要的atp敏感基底侧K传导。
From the* Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520; and‡ Department of Medicine, University of Vermont, Burlington, Vermont 05401 abstract The potassium conductance of the basolateral membrane (BLM) of proximal tubule cells is a critical regulator of transport since it is the major determinant of the negative cell membrane potential and is necessary for pump-leak coupling to the Na , K -ATPase pump. Despite this pivotal physiological role, the properties of this conductance have been incompletely characterized, in part due to difficulty gaining access to the BLM. We have investigated the properties of this BLM K conductance in dissociated, polarized Ambystoma proximal tubule cells. Nearly all seals made on Ambystoma cells contained inward rectifier K channels ( slope, in 24.5 0.6 pS, chord, out 3.7 0.4 pS). The rectification is mediated in part by internal Mg2 . The open probability of the channel increases modestly with hyperpolarization. The inward conducting properties are described by a saturating binding–unbinding model. The channel conducts Tl and K , but there is no significant conductance for Na , Rb , Cs , Li , NH4 , or Cl . The channel is inhibited by barium and the sulfonylurea agent glibenclamide, but not by tetraethylammonium. Channel rundown typically occurs in the absence of ATP, but cytosolic addition of 0.2 mM ATP (or any hydrolyzable nucleoside triphosphate) sustains channel activity indefinitely. Phosphorylation processes alone fail to sustain channel activity. Higher doses of ATP (or other nucleoside triphosphates) reversibly inhibit the channel. The K channel opener diazoxide opens the channel in the presence of 0.2 mM ATP, but does not alleviate the inhibition of millimolar doses of ATP. We conclude that this K channel is the major ATP-sensitive basolateral K conductance in the proximal tubule.