Nephron heterogeneity in renal excretion of sodium and potassium in the rat

Previous studies have demonstrated that net addition of sodium and potassium occurs between the late distal tubule and base of the papillary collecting duct during 10% body wt Ringer loading in the rat. The role of medullary structures in this phenomenon is not entirely clear, however. Therefore, micropuncture studies were performed to compare delivery of sodium and potassium to the late distal tubule of superficial nephrons, the papillary base, and papillary tip in control rats and animals in which papillary necrosis was induced 18-24 hr prior to study by the injection of bromoethylamine hydrobromide (BEA). Net addition of both sodium and potassium occurred between the late distal tubule and papillary base in Ringer-loaded control animals. BEA totally abolished the net addition of sodium between these sites, but net addition of potassium persisted. Total kidney GFR was reduced by nearly 50% in BEA rats, while nephron GFR was unaltered in superficial nephrons. Histologic studies demonstrated severe damage to loops of Henle, collecting ducts, and vasa recta within the papilla, but these structures appeared normal in the inner stripe of the outer medulla. In microinjection studies in which [³H]inulin was injected into surface tubules, urinary recovery of the isotope was virtually complete in BEA-treated rats (98.5%). This finding indicated that even in the presence of severe histologic damage, impermeability of the collecting duct to inulin was maintained, and calculation of fractional delivery of sodium and potassium to distal nephron sites is therefore valid. We conclude from these studies that the net addition of sodium between the late distal tubule and papillary base during Ringer loading is due to preferential decrease in sodium reabsorption in juxtamedullary nephrons. In contrast, the increment in potassium delivery between these sites is due to addition beyond the late distal tubule, probably by the cortical collecting tubule.