Cell swelling activates basolateral membrane Cl and K conductances in rabbit proximal tubule.
Cell swelling activates basolateral membrane Cl and K conductances in rabbit proximal tubule.
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细胞肿胀激活兔近曲小管基底外侧膜 Cl 和 K 电导。
DOI：
10.1152/ajprenal.1990.258.4.f951
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
O'Neil,RG
中科院分区：
文献类型：
--
作者：
Welling,PA;O'Neil,RG
在非灌注兔近端小管（S2段）的容量调节的离子基础进行了评估，通过使用同时测量小管体积通过视频光学成像技术和基底侧膜电压（Vbl）和相对离子电导通过传统的微电极。细胞体积（9.9 +/- 0.70 nl/cm小管长度）和Vbl（-42.8 +/- 3.6 mV）在对照等渗林格氏溶液（290 mosmol/kg）中保持稳定。当浸浴介质的渗透压降低至150 mosmol/kg时，小管在1分钟内膨胀至基线以上72%，随后在接下来的4-6分钟内调节至稳态，高于初始基线体积20 +/- 3%。细胞肿胀伴随着Vbl的瞬时超极化，为-14.3 +/- 2.0 mV（含HCO 3的林格氏液）和-10.0 +/- 0.7 mV（不含HCO 3的林格氏液）。尽管在碳酸氢盐缓冲液存在下钡不抑制超极化，但向无碳酸氢盐的林格氏液中加入2 mM Ba使Vbl去极化+22 mV，并消除了相对钾电导和伴随细胞肿胀的超极化（Δ Vbl = -4.6 +/-0.6 mV）。此外，K在基底侧膜的相对电导从等渗对照培养基中的0.16增加到细胞肿胀峰值时的0.34。由于Vbl的超极化后，细胞已肿胀约10%以上的基线，适度的阈值体积和时间延迟可能涉及触发的体积依赖性激活的K电导。在平行研究中，在等渗溶液中，Cl浴（49至4.9 mM）快速阶跃变化时Vbl的变化平均为5.3 +/- 1.0 mV，在细胞肿胀峰值时增加至+11.3 +/- 2.1（P小于或等于0.05）。这表示相对Cl电导增加0.08至0.20，这只能归因于基底外侧膜Cl电导的绝对增加，而不是其他主要基底外侧膜电导的减少。它的结论是，细胞肿胀的结果在Cl和K电导，这可能是随后的细胞体积调节的基础增加。
The ionic basis of volume regulation was assessed in the nonperfused rabbit proximal tubule (S2 segment) by use of simultaneous measurements of tubule volume via video-optical imaging techniques and basolateral membrane voltage (Vbl) and relative ionic conductance via conventional microelectrodes. Both cell volume (9.9 +/- 0.70 nl/cm tubule length) and Vbl (-42.8 +/- 3.6 mV) remained stable in the control isotonic Ringer solution (290 mosmol/kg). When the osmolality of the bathing medium was reduced to 150 mosmol/kg, tubules swelled 72% above base line within 1 min and subsequently regulated over the course of the next 4-6 min to a steady state 20 +/- 3% above the initial base-line volume. Cell swelling was accompanied by a transient hyperpolarization of Vbl of -14.3 +/- 2.0 mV (HCO3-containing Ringer) and -10.0 +/- 0.7 mV (HCO3-free Ringer). Although the hyperpolarization was not inhibited by barium in the presence of bicarbonate buffer, addition of 2 mM Ba to a bicarbonate-free Ringer depolarized Vbl by +22 mV and abolished both the relative potassium conductance and the hyperpolarization accompanying cell swelling (delta Vbl = -4.6 +/- 0.6 mV). Furthermore, the relative conductance of K at the basolateral membrane increased from 0.16 in the isotonic control medium to 0.34 at the peak of cell swelling. Because the hyperpolarization of Vbl ensued after cells had swollen approximately 10% above base line, a modest threshold volume and time delay may be involved in triggering the volume-dependent activation of the K conductance. In parallel studies, the change in Vbl on a rapid step-change in bath Cl (49 to 4.9 mM) averaged 5.3 +/- 1.0 mV in the isotonic solution and increased to +11.3 +/- 2.1 (P less than or equal to 0.05) at the peak of cell swelling. This represented an increase in the relative Cl conductance of 0.08 to 0.20, which could only be attributed to an absolute increase in the basolateral membrane Cl conductance and not to a reduction in the other major basolateral membrane conductances. It is concluded that cell swelling results in an increase in both Cl and K conductance, which may underlie subsequent cell volume regulation.