Abstract
Studies on isolated perfused rat hearts indicate that uric acid together with other dephosphorylated purine metabolites is released into the perfusate where it represents the major degradation product of purine nucleotidcs under basal conditions (Ronca-Testoni and Borghini, 1982a). During hypoxia, anoxia or ischaemia a very strong increase in purine release has been observed but in these conditions the contribution of the other purine derivatives (inosine and adenosine) to total purine release is higher than that of uric acid (Achterberg et al., 1986). The ability of the rat heart to degrade adenine compounds down to uric acid is explained by the presence of xanthine oxidase in the heart and recently this enzyme has been seen mainly localized on vascular endothelial cells (Gerlach et al., 1985). These cells as well as cardiomyocytes exhibit synthesis of purine nucleotides by active salvage pathways, in particular through hypo-xanthine guanine phosphoribosyltransferase (HGPT, EC 2.4.2.8) activity. Xanthine oxidase partially subtracts the purine ring from the salvage pathways.
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© 1989 Plenum Press, New York
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Ronca, G. et al. (1989). Uric Acid and Purine Compounds in Aortic and Coronary Sinus Blood in Man. In: Mikanagi, K., Nishioka, K., Kelley, W.N. (eds) Purine and Pyrimidine Metabolism in Man VI. Advances in Experimental Medicine and Biology, vol 253A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5673-8_63
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DOI: https://doi.org/10.1007/978-1-4684-5673-8_63
Publisher Name: Springer, Boston, MA
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