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Role of NO in Hyperuricemia induced Cardiac Metabolic Dysfunction in Pregnancy.
Author(s) -
MartinFernandez Beatriz,
Song Su,
Huang HarEr,
Hintze Thomas
Publication year - 2010
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.24.1_supplement.984.10
Subject(s) - medicine , endocrinology , xanthine oxidase inhibitor , blood pressure , bradykinin , xanthine oxidase , hyperuricemia , uric acid , allopurinol , chemistry , biochemistry , receptor , enzyme
Hyperuricemia (HU) causes cardiovascular dysfunction and is associated with many complications during pregnancy related to reduced NO bioactivity and high blood pressure (BP). This study assessed the mechanisms of HU on the NO‐dependent control of cardiac O 2 consumption in pregnant rats. Pregnant rats were fed oxonic acid (OA), an uricase inhibitor, (750mg/Kg body weight/day) by gavage (OA group) and allopurinol (AL), a xanthine oxidase inhibitor (OAA group), was placed in drinking water (150mg/L) every day for 20 days. OA increased significantly mean blood pressure (89.91±7.8 to 110.38±5.6 mmHg), heart weight/body weight ratio (0.24±0.01 to 0.26±0.01g/100g) and total peripheral resistance (1.15±0.15 to 1.55±0.17 mmHgmin −1 m −1 ). Treatment with AL reduced this response. The ability of bradykinin and carbachol to reduce myocardial O 2 consumption in vitro was impaired by 70% and 50%. The response was restored by tiron, tempol and apocynin. Pregnant rats fed L‐NAME also have impaired ability of bradykinin and carbachol to regulate myocardial O 2 consumption (59% and 62%). In summary, HU induces hypertension, increases O 2 production and reduces the ability of NO to regulate myocardial O 2 consumption in pregnancy. Supported by HL43023, 50142.