Effect of chronic hyperaldosteronism on the electrophysiology of rat distal colon.

Abstract

Microelectrodes have been used to study the effects of aldosterone on the barriers and forces controlling sodium and potassium transport in rat distal colon. Compared to control tissues, hyperaldosteronism induced by dietary sodium depletion resulted in a 7-fold increase in transepithelial voltage (VT) and a 52% decrease in total resistance (RT). Increased VT reflected both a rise in the basolateral membrane voltage (Vbl) and a fall in the apical membrane voltage (VA). RT was resolved into its separate membrane components using nystatin (585 U X ml-1), and the decrease in RT produced by aldosterone was found to be due entirely to a 66% decrease in the apical membrane resistance (RA). Amiloride had no effect on the control tissues, but restored VT, Vbl and VA in tissues from sodium deprived animals to control values. Amiloride also increased RT in the experimental tissue, but the post-amiloride values remained significantly lower than those in controls. These results indicate, therefore, that hyperaldosteronism results in an increase in VT by hyperpolarizing the basolateral membrane, as well as depolarizing apical membrane in rat distal colon. The fall in RT, however, is due only to a fall in RA since Rbl and junctional resistance (Rj) were unaffected. The data are consistent with the concept that aldosterone acts to stimulate sodium absorption by increasing the rate of cell entry of sodium, through the induction of amiloride-sensitive sodium channels in the apical membrane, and enhances the rate of potassium secretion by increasing the electrical driving force towards the mucosal solution.