Failure of potassium adaptation in vivo in the colon of aldosterone-deficient rats.

Prolonged potassium loading results in an adaptive change in colonic epithelium that increases the capacity for potassium excretion. We evaluated the role of aldosterone in colonic potassium adaptation, because potassium loading also increases the production of aldosterone. Experiments were performed in intact animals and in adrenalectomized rats with a high potassium intake replaced over a prolonged period with low physiologic amounts of corticosterone to provide a stable plasma level of 3 to 5 micrograms/dl. Net electrolyte movement and transmural potential difference were measured by an in vivo luminal perfusion technique. Compared with the rate of potassium secretion of -3.6 +/- 0.5 mu Eq/min/gm dry weight in potassium-loaded rats with intact adrenal glands, net secretion was significantly impaired (P less than 0.025) in potassium-loaded adrenalectomized animals with only corticosterone replacement (-1.1 +/- 0.5 mu Eq/min/gm dry weight). The rate in adrenalectomized animals, however, was comparable to that in intact animals receiving a normal potassium intake (0.3 +/- 0.2 mu Eq/min/gm dry weight). In addition, in intact animals prolonged potassium loading significantly increased transmural potential difference to -68 +/- 6 mV (P less than 0.005), compared with that in adrenalectomized, corticosterone-replaced, potassium-loaded animals (-30 +/- 4 mV) and intact animals with a normal intake of potassium (-25 +/- 7 mV). Net sodium absorption was reduced in aldosterone-deficient animals compared with the value in control and potassium-loaded animals with intact adrenal glands. These data indicate, therefore, that potassium adaptation is not induced in the absence of aldosterone and suggest that hyperaldosteronism plays an important role in induction of colonic potassium adaptation.