Abstract
Summary
The present experiments demonstrate that raising renal perfusion pressure in the isolated kidney caused a significant increase in sodium excretion in the absence of detectable changes in proximal tubule sodium transport suggesting that the natriuresis resulted primarily from a decrease in sodium transport along more distal nephron segments. The constancy of SNGFR/Cin argues against a role for redistribution of glomerular filtrate in the natriuresis.
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