Aldosterone stimulation of sodium transport

Abstract

On the basis of current concepts of the basic components of the Na + transport system across epithelial structures, we inferred that aldosterone could stimulate Na + transport in one of three ways: (1) by facilitating the entry of Na + into the effector epithelial cells, as vasopressin is believed to do, (2) by increasing the intrinsic activity of the Na + pump, or (3) by increasing the local concentration of the high-energy intermediate of the Na + pump. Three sets of experimental results were presented: (1) The response of the isolated toad bladder to vasopressin and to aldosterone under conditions of substrate depletion. (2) The effect of aldosterone on the response of the Na t transport system to saturating concentrations of vasopressin. (3) The effect of aldosterone on the Na + flux ratio during reversed net flow of Na + produced by a fixed serosal to mucosal electrical potential difference of 100 mV (serosa positive) and a 1:5 mucosal to serosal Na + concentration gradient. We found that in substrate-depleted hemibladders, aldosterone had no effect on Na + transport but vasopressin produced the usual rise. In substrate-enriched hemiblandders, the absolute increase in active Na + transport in response to vasopressin was greater after maximum stimulation by aldosterone than in control hemibladders. During steadily maintained reversed net flow of Na +, aldosterone produced a significant increase in the Na + flux ratio. These results support the concept that aldosterone increases the output of the Na + pump independently of an effect on the permeability of the mucosal surface epithelial cell.