These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Na+/Ca2+ exchanger inhibitor ameliorates impaired endothelium-dependent Na+ relaxation induced by high glucose in rat aorta.
    Author: Su Y, Liu XM, Sun YM, Jin HB, Luan Y, Wu Y.
    Journal: Clin Exp Pharmacol Physiol; 2008 Oct; 35(10):1265-70. PubMed ID: 18637014.
    Abstract:
    The present study was designed to investigate the effects of KB-R7943, an inhibitor of the Na+/Ca2+ exchanger, on impaired endothelium-dependent relaxation (EDR) induced by high glucose in rat isolated aorta. 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. 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 micromol/L) and high glucose for 24 h, significantly attenuation of impaired EDR was observed. This protective effect of KB-R7943 (10 micromol/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 (O2(-)) production in aortic tissue. KB-R7943 significantly decreased O2(-) production and increased SOD activity and NO release. 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.
    [Abstract] [Full Text] [Related] [New Search]