Interaction between the basolateral K+ and apical Na+ conductances in Necturus urinary bladder.
Experimental modulation of the apical membrane Na+ conductance or basolateral membrane Na+-K+ pump activity has been shown to result in parallel changes in the basolateral K+ conductance in a number of epithelia. To determine whether modulation of the basolateral K+ conductance would result in parallel changes in apical Na+ conductance and basolateral pump activity, Necturus urinary bladders stripped of serosal muscle and connective tissue were impaled through their basolateral membranes with microelectrodes in experiments that allowed rapid serosal solution changes. Exposure of the basolateral membrane to the K+ channel blockers Ba2+ (0.5 mM/liter), Cs+ (10 mM/liter), or Rb+ (10 mM/liter) increased the basolateral resistance (Rb) by greater than 75% in each case. The increases in Rb were accompanied simultaneously by significant increases in apical resistance (Ra) of greater than 20% and decreases in transepithelial Na+ transport. The increases in Ra, measured as slope resistances, cannot be attributed to nonlinearity of the I-V relationship of the apical membrane, since the measured cell membrane potentials with the K+ channel blockers present were not significantly different from those resulting from increasing serosal K+, a maneuver that did not affect Ra. Thus, blocking the K+ conductance causes a reduction in net Na+ transport by reducing K+ exit from the cell and simultaneously reducing Na+ entry into the cell. Close correlations between the calculated short-circuit current and the apical and basolateral conductances were preserved after the basolateral K+ conductance pathways had been blocked. Thus, the interaction between the basolateral and apical conductances revealed by blocking the basolateral K+ channels is part of a network of feedback relationships that normally serves to maintain cellular homeostasis during changes in the rate of transepithelial Na+ transport.
D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000494:pharmacology; D001693:Biological Transport, Active; D002451:Cell Compartmentation; D002462:Cell Membrane / Q000502:physiology; D002586:Cesium / Q000494:pharmacology; D004594:Electrophysiology; D004848:Epithelium / Q000502:physiology / Q000648:ultrastructure; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D009337:Necturus / Q000502:physiology; D011188:Potassium / Q000502:physiology*; D012413:Rubidium / Q000494:pharmacology; D012964:Sodium / Q000502:physiology*; D001743:Urinary Bladder / Q000502:physiology*; D014700:Verapamil / Q000494:pharmacology
D007473:Ion Channels; D002586:Cesium; D001464:Barium; D000584:Amiloride; D012964:Sodium; D014700:Verapamil; D012413:Rubidium; D011188:Potassium