Aldosterone-induced sodium transport in lower intestine

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Abstract
1. Short-circuit current (SCC) and electrical potential difference (PD) were measured in two epithelia of the lower gut of the domestic fowl, coprodeum and colon, mounted in vitro in the Ussing-chamber. The birds were suddenly switched from a low-NaCl to a high-NaCl diet, and 24 h aldosterone treatment (3×42.7 μg/kg i.m.) given from zero to 5 days after dietary change. 2. The effects on SCC and PD of addition of amino acids, and later amiloride, to the bathing media were measured, because a low-NaCl-diet which releases endogenous aldosterone, inhibits amino acid stimulation (in colon) and induces amiloride inhibition of SCC and PD (in both coprodeum and colon). 3. Birds were slaughtered 4 h after the last injection as single injections of aldosterone showed maximal change of SCC and PD, and maximal amino acid and amiloride effects, at that time. Control intramuscular injections of aldosterone showed a mono-exponential decline of the plasma concentration with a half time of 47 min. 4. In colon the aldosterone treatment induced the low-NaCl diet pattern of the transport parameters regardless of the delay after resalination. In coprodeum SCC declined gradually with time and reached 25% of the value at low-NaCl diet when aldosterone was given 5 days after resalination. 5. The data suggest that colon maintains a high flush of sodium through the epithelial cells regardless of whether the entry is via the amiloride-blockable sodium channel or the non-electrolyte stimulated pathway. In coprodeum aldosterone acts rapidly in opening the channels of the apical membrane, but needs longer time to activate the basolateral transport system. This is inactivated when the rate of sodium entry is low on the high-NaCl diet.