Mineralocorticoid regulation of sodium and potassium transport by the cortical collecting duct.

Chronic high-dose mineralocorticoid hormone treatment of rabbits results in marked alterations of the structure and function of the cortical collecting duct. Most importantly, the reabsorption of Na+ and the secretion of K+ are increased. Intracellular microelectrode measurements provide evidence consistent with the idea that the increased transport of these ions is a result of changes in the membrane conductances and electrochemical driving forces for passive ion movement and of the activity of the Na+,K+-ATPase. Specifically, the Na+ and K+ conductances of the apical membrane are increased, and the cellular potential profile is altered to promote transcellular movement of K+ from the peritubular to the luminal fluid compartments. The associated increase in the activity of the Na+,K+-ATPase facilitates extrusion of Na+ from and accumulation of K+ into the cell. The resistance of both the apical and basolateral cell membranes are reduced with DOCA treatment, while the resistance of the paracellular pathway is increased. Consequently, the electrophysiological properties of the tubule epithelium reflect to a greater degree the properties of the transcellular pathway.