Is thromboxane a potent antinatriuretic factor and is it involved in the development of acute renal failure?
Glycerol-treated rats exhibited significantly increased urinary thromboxane B2(TXB)2, prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1 alpha (6kPGF1 alpha) excretion and urine volume (UV). These increases were associated with significant decreases in creatinine clearance (CCr), urinary sodium concentration (UNa), urinary sodium excretion (UNaV), and fractional excretion of sodium (FENa%), which is consistent with the development of the prerenal (reversible) phase of acute renal failure (ARF). When glycerol-treated rats were pretreated with a selective inhibitor of thromboxane A2 (TXA2) synthesis (imidazole), urinary PGE2 and 6kPGF1 alpha excretion and UV remained unchanged, whereas CCr, UNa, UNaV decreases were partially prevented. Additionally, FENa% was increased, indicating inhibition of sodium reabsorption. The findings indicate that inhibition of TXA2 synthesis increases UNaV and partially improves CCr in glycerol-treated rats. Further histologic observation and functional follow-up over longer periods of time are needed to clarify the role of TXA2 in the development of ARF.
D058186:Acute Kidney Injury / Q000209:etiology*; D000818:Animals; D003404:Creatinine / Q000378:metabolism; D005260:Female; D005990:Glycerol / Q000633:toxicity; D007093:Imidazoles / Q000494:pharmacology; D009318:Natriuresis / Q000187:drug effects*; D011453:Prostaglandins / Q000652:urine; D051381:Rats; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors / Q000502:physiology*
D007093:Imidazoles; D011453:Prostaglandins; D013928:Thromboxane A2; C029899:imidazole; D003404:Creatinine; D005990:Glycerol