Mineralocorticoid regulation of apical cell membrane Na+ and K+ transport of the cortical collecting duct

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Abstract
The effects of mineralocorticoid (DOCA[deoxycorticosterone acetate]) treatment of rabbits on the Na+ and K+ transport properties of the cortical collecting duct apical cell membrane were assessed using microelectrode techniques. Applying standard cable techniques and equivalent circuit analysis to the isolated perfused tubule, the apical cell membrane K+ and Na+ currents and conductances could be estimated from the selective effects of the K+ channel blocker Ba2+ and the Na+ channel blocker amiloride on the apical membrane; amiloride treatment decreased the tight junction conductance by an average of 10%. After 1 day of DOCA treatment, the Na+ conductance and current (Na+ influx) of the apical cell membrane doubled and remained elevated with prolonged treatment for up to 2 wk. The apical cell membrane K+ conductance was not influenced after 1 day, although the K+ current (K+ secretion) increased significantly due to an increased driving force for K+ exit. After 4 days or more of DOCA treatment the K+ conductance doubled, resulting in a further modest stimulation in K+ secretion. After 2 wk of DOCA treatment the tight junction conductance decreased by near 30%, resulting in an additional hyperpolarization of the transepithelial voltage, thereby favoring K+ secretion. The actue effect (within 1 day) of mineralocorticoids on Na+ and K+ transport is an increase in the apical membrane Na+ conductance followed by delayed chronic alterations in the apical membrane K+ conductance and tight junction conductance; thereby this results in a sustained increased capacity of the tubule to reabsorb Na+ and secrete K+.

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