1. The purpose of this study was to evaluate the renal mechanisms which lead to a high urine [K+] in adrenalectomized (ADX) rats devoid of aldosterone.

2. By dividing the urine [K+] by the urine to plasma osmolality ratio, the [K+] in the cortical collecting duct luminal fluid can be estimated; dividing this value by the plasma [K+] yields an index of the transtubular [K+] gradient (TTKG) in vivo.

3. The TTKG was close to 7 in aldosterone deficient ADX rats while on a normal K+ diet and fell towards unity when amiloride or a low K+ diet was administered to these rats.

4. With a longer time on a low K+ diet, the TTKG was less than 1 in ADX rats. This suggests that K+ was reabsorbed in the medullary collecting duct under these conditions.

5. Hyperkalemia appears to have an ‘aldosterone-like’ action in the cortical collecting duct in vivo in the absence of aldosterone in ADX rats. This action of hyperkalemia permits normal K+ excretion rates despite the absence of mineralocorticoids.

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