Abstract
SummaryThe effect of aspirin on Epo formation was studied in normal Wistar rats and rats with hereditary hydronephrosis in which, due to renomedullary damage, PGs synthesis by the kidney is supposedly diminished. The obtained results show that, in Wistar rats exposed to a hypoxic stimulus, aspirin effectively diminishes Epo formation, presumably by inhibiting PGs synthesis. Under the same conditions aspirin failed to abolish Epo production in rats with hereditary hydronephrosis. No difference in Epo formation was found between control Wistar and control hydronephrotic rats when exposed to a hypoxic stimulus. The presented results indicate that renal PGs are a contributory factor in the mechanism of hypoxia-induced Epo production, rather than the controlling one.
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