Hypotonicity activates a lanthanide-sensitive pathway for K + release in A6 epithelia

• Published in: American Journal of Physiology: Cell Physiology 1998-07, Vol.275 (1), p.C189
• Main Authors: De Smet, Patrick, Li, Jinqing, Van Driessche, Willy
• Format: Article
• Language: English
• ISSN: 1522-1563
• DOI: 10.1152/ajpcell.1998.275.1.C189

The nature of the pathway for K release activated during regulatory volume decrease (RVD) in A6 epithelia was investigated by measuring cell thickness (T ) as an index of cell volume and by probing K efflux with Rb as tracer for K (R ). Cell swelling was induced by sudden reduction of basolateral osmolality (from 260 to 140 mosmol/kgH O). Experiments were performed in the absence of Na transport. Apical R was negligible in iso- and hyposmotic conditions. On the other hand, osmotic shock increased basolateral R ([Formula: see text]) rapidly, reaching a maximum 7 min after the peak in T . Quinine (0.5 mM) completely inhibited RVD and [Formula: see text]. Also verapamil (0.2 mM) impeded volume recovery considerably; lidocaine (0.2 mM) did not exert a noticeable effect. The K channel blocker Ba (30 mM) delayed RVD but could not prevent complete volume recovery. Cs inhibited RVD noticeably at concentrations 40 mM), the initial osmometric swelling was followed by a gradual increase of T , suggesting activation of Cs influx. Chronic exposure of the basolateral surface to 0.5 mM La or Gd completely abolished RVD and[Formula: see text]. Acute administration of lanthanides at the time of osmolality decrease did not affect the initial phase of RVD and reduced [Formula: see text]only slightly. Apical Gd exerted an inhibitory effect on RVD and [Formula: see text]. The effect of Gd should therefore be localized at an intracellular site. The role of Ca entry could be excluded by failure of extracellular Ca removal to inhibit volume recovery. In contrast to lanthanides, chronically and acutely administered Mg (0.5 mM) inhibited RVD and[Formula: see text] by ∼50%. These data suggest that K excretion during RVD occurs through a rather poorly selective pathway that does not seem to be directly activated by membrane stretch.