Idiopathic pulmonary arterial hypertension (IPAH) is believed to be made worse by oxidative stress. The enzyme, xanthine oxidase, contributes to that oxidative stress, causing damage to arteries by increasing uric acid levels. High uric acid levels (hyperuricemia) in IPAH are believed to be the result of increased xanthine oxidase activity. The xanthine oxidase enzyme is bound to the surface of cells by glycosaminoglycans and is released from them by heparin.
The authors studied 53 patients (men and women) with IPAH. Pulmonary pressures were measured and blood samples were tested for uric acid and for xanthine oxidase activity. The results were that xanthine oxidase activity was found to be increased in patients with IPAH. There was no relationship between the xanthine oxidase levels and the pulmonary arterial pressures and oxygen levels.
CONCLUSION: Elevated levels of xanthine oxidase are seen in patients with IPAH and may be the cause of the vascular disease that is associated with IPAH. Further testing will show the value of phospodiesterase inhibitors and other treatments in IPAH.
NOTE: Xanthine oxidase is the enzyme necessary for the production of uric acid from precursor chemicals. Blocking xanthine oxidase enzyme reduces the symptoms of gout. Natural agents to treat elevated uric acid elevation include flavonoids, black tea, figs, astragulus, cocoa and white mulberry twig. Arginine is beneficial in the treatment of pulmonary hypertension, Raynaud’s arteritis and sickle cell disease. Read about the ability of Phyllanthus niruri to inhibit xanthine oxidase.
Fructose should be avoided, especially, when there is high uric acid. Fructose will further increase the uric acid levels.
Quercitin is a phosphodiesterase inhibitor, as is viagra. Flavonoids are xanthine oxidase inhibitors and phosphodiesterase inhibitor.
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