Potassium depletion: renal membrane lipid metabolism and Na/H exchanger abundance in aged F344 x BNF1 rats.

Potassium depletion (-K) is a common electrolyte abnormality in elderly humans, occurring after diuretic use or poor oral intake. We hypothesized that aging would result in an increase in renal membrane lipid metabolism in both control and -K, and that the Na/H exchanger's protein abundance to -K would be blunted. Young and senescent non-obese male Fisher 344 x Brown-Norway F1 rats (F344 x BNF1) were fed either a normal or a K-deficient diet for 7 days. At 24-h, 32P incorporation was measured for renal cortical brush-border (BBM) and basolateral membrane (BLM) lipid metabolism. All -K animals showed a reduction in total body potassium stores, a fall in plasma aldosterone, a urinary concentrating defect, and an increase in plasma cholesterol and urine ammonium excretion (p < .001). In BBM of both age groups, -K increased phosphatidylserine, sphingomyelin, phosphatidylcholine, and phosphatidylethanolamine concentrations, but 32P incorporation fell. In BLM of young K-depleted rats, however, only phosphatidylcholine concentration increased. In the hypokalemic aged rats, the concentration of all BLM phospholipids rose, whereas 32P incorporation fell. In both membranes, cholesterol concentration and the molar ratio of cholesterol to total phospholipid increased with -K (p < .05). Potassium depletion caused brush-border membrane NHE-3 protein abundance to rise, but only in the young rats. Neither NHE-3 nor basolateral NHE-1 protein abundance was affected in aged animals with -K. These results provide the first evidence, in non-obese aged rats, that selective age-associated modifications occur in membrane lipid metabolism and membrane transporter protein abundance during -K. That aging causes a maladaptive response in brush-border NHE-3 protein expression may have important implications for elderly humans, particularly if they are given diuretics and become potassium depleted.