Abstract
Serum gastrin activity was determined in rats 48 hr after bilateral nephrectomy or bilateral ureteral ligation. Although both groups of rats became equally azotemic as determined by serum urea nitrogen levels, serum gastrin levels were elevated only in the rats with bilateral nephrectomies, above the levels observed in normal or sham-operated control rats. These data (1) suggest that hypergastrinemia of renal failure is related to the loss of normal functioning renal mass and is not a result of the uremic state per se, and (2) provide additional evidence supporting the role of the kidney as a major site of degradation of endogenous gastrin in the rat.
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