American Journal of Physiology-Legacy Content · 1963 · 64 citations · 0 references
MedicineNephrologyPhysiologyExcretionMineral MetabolismRenal PathophysiologyGlomerular FiltrationRenal ExcretionRenal HemodynamicsRenal PhysiologySodium BalanceUrinary ExcretionCompensatory MechanismsCompensatory Renal FunctionProximal Tubular Mineral ReabsorptionSodium Transport RegulationTubular Reabsorption BalanceTubular Sodium ReabsorptionUrinary Potassium Excretion
In normal male rats infused intravenously with 0.1–0.9 ml/kg min 0.15 m NaCl, urine flow increased with the rate of infusion, and C In increased as a linear function of urine flow. After functional exclusion of one kidney, "compensatory hyperfunction," defined as a permanent increase in glomerular filtration rate ( GFR), began during the 2nd week. Changes in the functions of the remaining kidney occurring earlier than any increase in GFR are termed "compensatory adaptation." The main change noted in compensatory adaptation was a decrease in tubular sodium reabsorption followed by a nearly doubled rate of urine flow and large increases in sodium and potassium excretion. The fall in hematocrit value was the same as in controls. Compensatory adaptation began during the 1st hr, and was complete 2 hr after removing one kidney or ligating one ureter. Changes in renal functions after both types of operation were indistinguishable. Maximum urinary concentration in dehydrated rats treated with vasopressin was not depressed during compensatory adaptation, although urine flow per kidney was doubled.