Sackin H
Department of Physiology and Biophysics, Cornell University Medical College, New York, New York 10021.
Am J Physiol. 1987 Dec;253(6 Pt 2):F1253-62. doi: 10.1152/ajprenal.1987.253.6.F1253.
A short open-time potassium (K) channel that has previously been identified in the basolateral membrane of Necturus proximal tubule (17) is activated by membrane stretch. Application of between 12 and 20 cmH2O negative pressure to the patch pipette reversibly increases mean number of open basolateral K channels (NP0) by a factor of 5.3 +/- 2 in cell-attached patches (n = 4) and a factor of 13.7 +/- 5 in excised patches (n = 8). This stretch activation does not alter channel selectivity or conductance and depends on neither the direction of K current nor the orientation of the patch ("inside-out" vs. "outside-out"). The increase in NP0 occurs within seconds after applying negative pressure to the patch and is proportional to applied negative pressure. Stretch activation of the basolateral potassium channel may play an important role in proximal tubule cell volume regulation. For example, if swelling stretches the basolateral membrane, the resulting increase in NP0 could restore cell volume by loss of K (with an accompanying anion) followed by osmotic exit of water.
先前已在美西螈近端小管基底外侧膜中鉴定出的一种开放时间较短的钾（K）通道可被膜拉伸激活。向膜片吸管施加12至20 cmH₂O的负压会使细胞贴附式膜片中基底外侧K通道的平均开放数量（NP₀）可逆地增加5.3±2倍（n = 4），在切除式膜片中增加13.7±5倍（n = 8）。这种拉伸激活不会改变通道的选择性或电导，并且既不依赖于K电流的方向，也不依赖于膜片的取向（“内向外”与“外向内”）。在对膜片施加负压后的几秒钟内NP₀就会增加，并且与施加的负压成正比。基底外侧钾通道的拉伸激活可能在近端小管细胞体积调节中起重要作用。例如，如果肿胀使基底外侧膜拉伸，由此导致的NP₀增加可通过K（伴随阴离子）的丢失，随后水的渗透流出，来恢复细胞体积。
