Abstract
It has been demonstrated by several recent studies that saline loading in the dog may result in decreased net tubular reabsorption of sodium independent of mineralocorticoids (1–5). On the basis of recent studies from this laboratory it was suggested that decreased tubular reabsorption of sodium during saline loading may result in part from an increased renal medullary blood flow(4,5). Increased medullary blood flow should decrease medullary interstitial hyper tonicity, and, in turn, the passive loss of water from the descending limb of Henle' Loop should diminish. The resulting increased rate of flow of fluid with a lower concentration of sodium could limit the absolute reabsorption of sodium by the ascending limb (4,5). If extracellular volume expansion does increase renal medullary blood flow, and if the reabsorption of sodium by the ascending limb of Henle' Loop is influenced by the concentration of sodium in the tubular fluid, then the concentrating mechanism (as measured by TcH2O) should be influenced by both extracellular volume expansion and by the concentration of sodium in the glomerular filtrate. The present studies were designed to compare the concentrating capacity during different types of solute loading and during different degrees of extracellular volume expansion. It was observed that at high rates of solute excretion the concentrating mechanism was less efficient during isotoinc saline loading than during hypertonic mannitol loading, and that hypertonic saline loading was associated with even more efficient urinary concentration than observed with hypertonic mannitol.
Methods. Experiments were performed in 6 unanesthetized female mongrel dogs (weighing 19 to 21 kg) trained to stand with the support of loose slings. Animals were deprived of water for 2 days and of food the day before experiments. Vasopressin (Pitressin® tannate) in oil 5 units and desoxycorticosterone acetate (DOCA) 10 mg were given intramuscularly 12–18 hours before the experiments.
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