Urinary inhibitor of the ammoniagenic response to acute XXXX is a prostaglandin.

@entity12906 @entity1160 @entity5728 @entity1421 @entity3009 @entity520 @entity3774 @entity35 @entity3352 @entity3655
Both @entity12906 and acute @entity520 stimulate @entity3655 production by the isolated perfused @entity35 kidney. This stimulatory effect is abolished if the urine is drained back into the recirculating perfusate rather than collected. To determine whether the urinary inhibitor is a cyclooxygenase product, studies were carried out using prostaglandin synthetase inhibitors. Kidneys perfused with 0.5 mmol/L @entity1160 and urine reinfusion were subjected to @entity12906 (30% CO2, pH 6.8). With either @entity3352 (20 mumol/L) or @entity5728 (20 mumol/L) in the perfusate, @entity3655 production increased significantly in response to @entity12906 despite urine reinfusion. The increment in @entity3655 production was comparable to that in studies with urine collection, indicating that a cyclooxygenase product can account completely for the urinary inhibitor. To further characterize the urinary prostaglandin inhibitor, studies were performed with both the isolated perfused kidney and renal cortical tubules. @entity1421 ( @entity1421 ) did not exhibit an inhibitory effect on @entity3655 production with either experimental model. @entity3774 at low doses inhibited @entity3655 production in response to acute @entity520 by the isolated kidney, but an effect was not apparent with higher concentrations. PGF2 alpha inhibited the stimulatory effect of a low pH (7.1) on @entity3655 production by isolated tubules, and had no effect on ammoniagenesis at pH 7.4. Thus a @entity3009 , which is not @entity1421 and may be PGF2 alpha, appears to be the previously unidentified urinary inhibitor of the ammoniagenic response to acute @entity520 found with the isolated perfused kidney.
