科研之友
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摘要
Uric acid (UA) results from xanthine oxidase (XO) catabolism of xanthine and is the final product of purine catabolism in humans. In this species, hyperuricemia is associated with gout, nephropathy, and increased cardiovascular disease risk. Although the effects of hyperuricemia in vascular biology are overall controversial, UA has been described as an antioxidant and as potentially improving endothelial function. Hypertension is associated with endothelial dysfunction. We hypothesized that UA improves the endothelial function of aorta from deoxycorticosterone acetate (DOCA)-salt hypertensive rats. UA (100 mu M) in the presence of the uricase inhibitor oxonic acid (10 mu M) did not modify relaxation to acetylcholine (ACh) (1 nM-10 mu M) in the aorta from nontreated, sham normotensive, and DOCA-salt hypertensive rats [response to 10 mu M ACh for UA versus vehicle, respectively: nontreated = 37 +/- 7 versus 48 +/- 7%, sham = 53 +/- 15 versus 57 +/- 20%, DOCA = 81 +/- 4 versus 85 +/- 2% from 20 mu M prostaglandin 2 alpha (PGF(2 alpha))-induced contraction]. Allopurinol (100 mu M), a XO inhibitor, did not significantly alter the ACh-induced relaxation of sham and DOCA aortic rings (response to 10 mu M ACh for allopurinol versus vehicle, respectively: sham = 61 +/- 5 versus 68 +/- 9%, DOCA = 87 +/- 6 versus 88 +/- 3% from 20 mu M PGF(2 alpha)-induced contraction). Uricemia, ranging from unmeasurable to 547 mu M in sham and to 506 mu M in DOCA rats, was not significantly different between these two groups. The expression and activity of XO, as well as the expression of uricase, were not different between sham and DOCA rat aorta. We conclude that, at least in vitro, UA does not affect the ACh-induced relaxation of normotensive and DOCA-salt hypertensive rats.
- 出版日期2010-6
