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Na + /Ca 2+ EXCHANGER INHIBITOR AMELIORATES IMPAIRED ENDOTHELIUM‐DEPENDENT Na + RELAXATION INDUCED BY HIGH GLUCOSE IN RAT AORTA
Author(s) -
Su Ying,
Liu XiaoMin,
Sun YanMing,
Jin HongBo,
Luan Ying,
Wu Yun
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2008.05002.x
Subject(s) - chemistry , nitric oxide , superoxide dismutase , sodium nitroprusside , medicine , endocrinology , aorta , superoxide , endothelium , nitric oxide synthase , sodium , biochemistry , biophysics , oxidative stress , enzyme , biology , organic chemistry
SUMMARY1 The present study was designed to investigate the effects of KB‐R7943, an inhibitor of the Na + /Ca 2+ exchanger, on impaired endothelium‐dependent relaxation (EDR) induced by high glucose in rat isolated aorta. 2 Both acetylcholine (ACh)‐induced EDR and sodium nitroprusside (SNP)‐induced endothelium‐independent relaxation (EIR) were measured after aortic rings had been exposed to high glucose in the absence and presence of KB‐R7943. 3 Coincubation of aortic rings with high glucose (25 mmol/L) for 24 h resulted in a significant inhibition of EDR, but had no effect on EIR. After incubation of aortic rings in the presence of both KB‐R7943 (0.1–10 µmol/L) and high glucose for 24 h, significantly attenuation of impaired EDR was observed. This protective effect of KB‐R7943 (10 µmol/L) was abolished by superoxide dismutase (SOD; 200 U/mL) and l ‐arginine (3 mmol/L), whereas d ‐arginine (3 mmol/L) had no effect. Similarly, high glucose decreased SOD activity and the release of nitric oxide (NO) and increased superoxide anion () production in aortic tissue. KB‐R7943 significantly decreased production and increased SOD activity and NO release. 4 These results suggest that KB‐R7943 can restore impaired EDR induced by high glucose in rat isolated aorta, which may be related to the scavenging of oxygen free radicals and enhanced NO production.