Abstract
Summary
The renal excretion of sodium and other renal functions were studied in dogs during non-shocking hemorrhage, while renal arterial pressure was maintained constant by controlled partial mechanical obstruction of the aorta. In some experiments, one kidney was denervated beforehand. The excretion of sodium declined in the absence of measurable changes in glomerular nitration or renal plasma flow. The explanation is proposed that hemorrhage causes an intrarenal redistribution of blood flow which favors tubules with more than average sodium reabsorbing activity, although steroid effects on tubular function cannot be excluded.
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