Volume regulation following Na+ pump inhibition in CCT principal cells: apical K+ loss.
Volume regulation following Na+ pump inhibition in CCT principal cells: apical K+ loss.
复制标题
CCT 主细胞中 Na 泵抑制后的容量调节：顶端 K 损失。
DOI：
10.1152/ajprenal.1990.258.3.f732
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Strange,K
中科院分区：
文献类型：
--
作者：
Strange,K
哇巴因可使兔皮质集合管(CCT)主细胞肿胀67%。肿胀的细胞以4%/分钟的速度下调其体积，至比对照低16%的新体积。在肾小管周围加入2.0微米前列腺素E_2(PGE_2)，一种可能的内源性Na+泵抑制剂，也观察到了类似的肿胀和容量调节模式。2.0 mM Ba2+或5.0 mM TEA+可抑制哇巴因肿胀细胞调节性体积减小(RVD)50-70%。肾小管周围TEA+对RVD无影响。腔内加入5.0 mM TEA+或0.2 mM奎尼丁抑制RVD50-60%，提示参与心尖K+通道。这一通道似乎与静息状态下的心尖K+电导不同。用Rb+代替细胞内的K+，对哇巴因肿胀的速度和幅度几乎没有影响，但对RVD50-60%有抑制作用。腔内K+在哇巴因前或RVD完成后升高10倍，分别导致主细胞肿胀10%和31%。在对照细胞中，这种K(+)诱导的肿胀不受灌流液中1.0 mM奎尼丁的影响，可以通过增加Rb+而不是K+浓度来模拟。然而，体积调节的主细胞中的肿胀大小，通过存在腔内奎尼丁或通过腔内添加Rb+而不是K+来减少50%-60%。推测的顶端RVDK+通道可能与其他实验室的主细胞膜片钳研究中描述的高电导K+通道相似。
Ouabain caused rabbit cortical collecting tubule (CCT) principal cells to swell 67%. Swollen cells downregulated their volume at a rate of 4%/min to a new volume 16% below control. A qualitatively similar pattern of swelling and volume regulation was observed with peritubular addition of 2.0 microM prostaglandin E2 (PGE2), a putative endogenous Na+ pump inhibitor. Regulatory volume decrease (RVD) in ouabain-swollen cells was inhibited 50-70% by bilateral addition of 2.0 mM Ba2+ or 5.0 mM TEA+. Peritubular TEA+ had no effect on RVD. Luminal addition of 5.0 mM TEA+ or 0.2 mM quinidine inhibited RVD 50-60%, suggesting involvement of an apical K+ channel. This channel appeared to be distinct from the resting apical K+ conductance. Replacement of cellular K+ with Rb+, which is commonly used as a tracer of K+ secretion in the CCT, had little effect on the rate and magnitude of ouabain swelling but inhibited RVD 50-60%. A 10-fold elevation of luminal K+ before ouabain or after completion of RVD caused principal cells to swell 10% and 31%, respectively. In control cells, this K(+)-induced swelling was unaffected by the presence of 1.0 mM quinidine in the perfusate and could be mimicked by elevation of Rb+ instead of K+ concentration. The magnitude of swelling in volume-regulated principal cells, however, was reduced 50-60% by the presence of luminal quinidine or by luminal addition of Rb+ instead of K+. The putative apical RVD K+ channel may be similar to high-conductance K+ channels described in principal cell patch-clamp studies from other laboratories.