Aldosterone increases the maximal turnover rate of the sodium pump

Publisher Website
Google Scholar
Abstract
These experiments were performed to determine whether aldosterone-dependent effects in apical and basolateral membranes could be temporarily dissociated and whether aldosterone increases the maximal capacity, or maximum turnover rate of the sodium pump. Tissue from rat distal colon exposed to the action of high plasma levels of aldosterone for 4 h, 24 h and 7–10 days was compared to control tissue in a modified Ussing chamber, before and after addition of nystatin to the mucosal solution to remove the apical barrier to the cell entry of sodium. The maximum turnover rate of the sodium pump was represented by the equivalent short circuit current,I sc, after the addition of nystatin. After 4 h of aldosterone basalI sc increased 2.6-fold above control (43±34 μA·cm−2,pV T, increased 2-fold over control (−7.0±5.5 mV, lumen negative,pI sc (11-fold) and a fall inR T to 50% of control. Similar changes were observed after 7–10 days on low sodium diet, and at all time intervals the changes were completely inhibited by amiloride (10−4 M). Although aldosterone stimulatedI sc within 4 h, there was no further increase inI sc of nystatin during the same time period compared to the control post-nystatinI sc of 419±79 μA·cm−2. However, after 24 h aldosterone caused approximately a 40% increase in the maximal turnover rate of the sodium pump, which persisted for 7–10 days. These data support the interference that the effects of aldosterone in animals with intact adrenal glands to increase sodium transport are dissimilar in acute and chronic conditions. These experiments suggest that the acute action, observed within a few hours of exposure, is caused by apical membrane effects, while during chronic exposure for at least 24 h the increase in apical conductance and in number of sodium pumps in basolateral membrane act synergistically to augment sodium transport.