Induction of amiloride-sensitive sodium transport in the rat colon by mineralocorticoids

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Abstract
In contrast to that in many other species, the short-circuit current of the colon from normal rats is not inhibited by the diuretic amiloride. To evaluate the effects of mineralocorticoids on rat colonic electrolyte transport, aldosterone [ALDO] levels were raised in vivo by a Na-deficient diet, a diet high in K, dehydration, furosemide-induced diuresis, and exogenous mineralocorticoids. The ability of the short-circuit current to be inhibited by amiloride could be induced with a half time of 10-14 h after elevation of ALDO, and was prevented by simultaneous administration of spironolactone, a mineralocorticoid antagonist. Amiloride sensitivity was essentially complete in the descending colon (amiloride-inhibitable short-circuit current = 95 .+-. 4%), but was only partial in the ascending colon (20 .+-. 12%) and the cecum (15 .+-. 9%). Chronically high ALDO levels increased the short-circuit current in the descending colon 6-fold, the conductance 1.8-fold and the activity of Na-K-ATPase 1.8-fold. The half time for these changes was 7-10 days, suggesting that the colon responds to ALDO in 2 ways: initially by inducing the amiloride-sensitive Na transport system in the luminal membrane, and, after chronic treatment, by increasing the short-circuit current, the conductance, and the activity of Na-K-ATPase.

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