Role of aldosterone in the mechanism of potassium adaptation in the initial collecting tubule

Studies were performed on the initial collecting tubule of the rat to determine whether potassium adaptation in this nephron segment is aldosterone-dependent. Previous studies demonstrated that chronic potassium loading, in animals with intact adrenal glands, caused an increase in transepithelial potential difference in late distal convolution, an increase in surface density of the basolateral cell membrane, Sv(BLM), or principal cells in the initial collecting duct, and a rise in plasma aldosterone levels. The present study shows that epithelial changes that characterize dietary potassium loading are not dependent on hyperaldosteronism, since potential difference (-47 ± 1 vs. 40 ± 3 mV, lumen negative) and Sv(BLM) (2.91 ± 0.11 vs. 2.53 ± 0.09 μm²/μm³) increased significantly (P < 0.05) in the late distal convolution of adrenalectomized, hormone-replaced animals in which plasma aldosterone levels were maintained at basal values of approximately 5 ng/dl. In addition, these experiments suggest that the initial collecting tubule is sensitive to the action of aldosterone, at physiological plasma levels, since chronic hyperaldosteronism, in the absence of potassium loading, increased Sv(BLM) in initial collecting tubule cells. In contrast to other mineralocorticoid-sensitive tissues, however, neither the acute nor chronic administration of aldosterone caused an increase in potential difference in late distal convolution. These results suggest that the mechanism by which aldosterone stimulates electrolyte movement is not identical in all target tissues.