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Uric acid does not impact the endothelial‐dependent relaxation of aorta from normal and hypertensive rats
Author(s) -
Szasz Theodora,
Linder A Elizabeth,
Watts Stephanie W
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.965.5
Subject(s) - medicine , endocrinology , aorta , xanthine oxidase , uric acid , endothelial dysfunction , chemistry , contraction (grammar) , hyperuricemia , endothelium , enzyme , biochemistry
Vascular xanthine oxidase (XO) activity and superoxide, a product of this activity, increase in hypertension. Uric acid (UA), the other XO‐derived product, has a controversial role in modulating vascular reactivity. Hyperuricemia induces hypertension and endothelial dysfunction in rats. Endothelial‐dependent relaxation is decreased in aorta from deoxycorticosterone (DOCA)‐salt hypertensive compared to sham normotensive rats. We hypothesized that UA impairs endothelial‐dependent relaxation in aorta from DOCA rats. Uricemia, ranging from unmeasurable to 547 umol/L in sham and to 506 umol/L in DOCA rats, was not significantly different. UA (1 nM – 100 uM), in the presence of uricase inhibition (oxonic acid 10 uM), did not contract normal aorta. The same combination (100 uM UA, 10 uM oxonic acid) did not modify relaxation to ACh (1 nM – 10 uM) in the normal, sham and DOCA aorta, when compared to vehicle, respectively (response to 10 uM ACh: normal=37±7 vs 48±7, sham=53±15 vs 57±20, DOCA=81±4 vs 85±2 % 20uM PGF2α contraction). Allopurinol (100 uM), the XO inhibitor, did not significantly alter the ACh‐induced relaxation of sham and DOCA aortic rings, when compared to its vehicle (response to 10 uM ACh: sham=61±5 vs 68±9, DOCA=87±6 vs 88±3 % 20 uM PGF2α contraction). These data suggest that XO, at least through its UA arm, does not impact the endothelial function of aorta in normal conditions and in DOCA‐salt hypertension.