FUNCTIONAL PROFILE OF THE ISOLATED UREMIC NEPHRON - POTASSIUM ADAPTATION IN THE RABBIT CORTICAL COLLECTING TUBULE

As a renal function declines in patients and experimental animals with chronic renal disease, K homeostasis is maintained by a progressive increase in K secretion by the surviving nephrons, a phenomenon known as K adaptation. To determine the nephron site and the underlying mechanisms responsible for this phenomenon, studies were performed on normal and 75% nephrectomized rabbits maintained on normal or high-K diets. Cortical collecting tubules (CCT) were dissected from the normal and remnant kidneys and perfused in vitro in an artificial bath solution. In normal CCT mean (.+-. SE) net K secretion, JK [net potassium flux] (PEQ/cm per s) was 1.26 .+-. 0.43 (normal diet) and 3.27 .+-. 0.66 (high-K diet). In uremic CCT, JK was 3.55 .+-. 0.60 (normal diet) and 6.83 .+-. 0.58 (high-K diet). By reducing the dietary intake of K in proportion to the reduction of renal mass in these uremic animals, the adaptation in K secretion was prevented (JK: 1.22 .+-. 0.40). Transeptithelial potential difference was similar in CCT from normal and uremic animals on a normal diet despite the fact that JK was significantly greater in the latter group. In both normal and uremic CCT, the increase in JK caused by K loading was associated with an increase in luminal negativity. Plasma aldosterone levels were elevated only in the uremic-high K rabbits, suggesting that a mineralocorticoid effect on the CCT may be exaggerated when K loading is superimposed upon decreased excretory capacity. The activity of Na-K ATPase was comparable in normal and uremic CCT from rabbits on either normal or high-K diets, indicating that K adaptation may occur independently of changes in the activity of this enzyme. Intracellular potassium content measured chemically and by 42K exchange, was not significantly altered in either normal or uremic CCT when dietary K intake was increased, despite the fact the JK was increased under these circumstances. The CCT is an important site of K adaptation in the surviving nephrons of animals with reduced renal mass. This adaptation is an intrinsic property of the CCT and is expressed in the absence of a uremic milieu. K adaptation by the uremic CCT is not fixed according to the degree of compensatory hypertrophy, but varies according to the excretory requirements of the animals. Transeptihelial potential difference and circulating aldosterone levels contribute to the adaptation, but neither factor can entirely account for the phenomenon. K adaptation by the CCT occurs in the absence of changes in Na-K ATPase activity and intracellular K content.