Potassium conductances in tracheal epithelium activated by secretion and cell swelling.
Potassium conductances in tracheal epithelium activated by secretion and cell swelling.
复制标题
气管上皮中的钾电导由分泌和细胞肿胀激活。
DOI:
10.1152/ajpcell.1990.258.4.c630
复制
发表时间:
1990
期刊:
影响因子:
--
通讯作者:
Frizzell,RA
中科院分区:
文献类型:
--
作者:
Butt,AG;Clapp,WL;Frizzell,RA
Increased basolateral membrane K conductance accompanies stimulation of Cl secretion across canine trachea. To assess the K conductance properties, we permeabilized the apical membranes with amphotericin B and monitored the current and conductance caused by K flow across the basolateral membranes. Under basal unstimulated conditions, two K conductances could be distinguished by blockers. One was inhibited only by barium; the other was sensitive also to quinidine and lidocaine. The permeabilities of the basal conductance pathways to K and Rb were similar (PK/PRb approximately equal to 1.5). The secretory agonist, epinephrine, selectively increased the quinidine-insensitive conductance, implicating it in the Cl secretory response. Cell swelling induced a third conductance with a low permeability to Rb (PK/PRb approximately equal to 10) that was quinidine sensitive. In tissues not treated with amphotericin, neither quinidine nor Rb-for-K replacement inhibited transepithelial Cl secretion. Thus neither of the quinidine-sensitive K conductances (basal or swelling induced) contribute to the increase in basolateral K conductance during Cl secretion. Cell shrinkage inhibited all three conductances and secretion, suggesting that the initial priority of the cell is volume regulation.