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

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Abstract
Previous studies have demonstrated that net addition of Na and K 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. Micropuncture studies were performed to compare delivery of Na and K 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 h prior to study by the injection of bromoethylamine hydrobromide (BEA). Net addition of both Na and K occurred between the late distal tubule and papillary base in Ringer-loaded control animals. BEA totally abolished the net addition of Na between these sites, but net addition of K 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; these structures however 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 indicates that even in the presence of severe histologic damage, impermeability of the collecting duct to inulin was maintained, and calculation of fractional delivery of Na and K to distal nephron sites is therefore valid. Net addition of sodium between the late distal tubule and papillary base during Ringer loading is apparently due to preferential decrease in Na reabsorption in juxtamedullary nephrons. The increment in K delivery between these sites is due to addition beyond the late distal tubule, probably by the cortical collecting tubule.