A situation may arise where a person is deprived of both sodium and potassium, leading to a deficit of both ions. This will lead to the release of angiotensin II, which stimulates the production of aldosterone.
Angiotensin II enhances the reabsorption of bicarbonate in the proximal and distal tubules. The aldosterone opens the ENaC which leads to reabsorption of sodium. Increased delivery of bicarbonate distally results in increased secretion of H+ and the combination of this with increased sodium reabsorption leads to increased chloride reabsorption. This in turn means that the electrical gradient which leads to net potassium secretion, when sodium is reabsorbed in excess of chloride, does not appear.