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【期刊论文】Specific Potentiation of Endothelium-Dependent Contractions in SHR by Tetrahydrobiopterin
张寄南, Di Yang, , Nigel Levens, Ji Nan Zhang, Paul M. Vanhoutte, Michel F
Downloaded from hyper. Ahajournals org by on May 9, 2007,-0001,():
-1年11月30日
This study was designed to determine the effect of pteridines, R-and S-tetrahydrobiopterin, sepiapterin, and dihydrobiopterin on endothelium-dependent contractions to acetylcholine in isolated aortas from spontaneously hypertensive rat and normotensive Wistar-Kyoto rat. The noncumulative addition of redox-active pteridines R- and S-tetrahydrobiopterin (but not the oxidized analogues sepiapterin and dihydrobiopterin) produced a concentrationdependent transient contraction in isolated aortic rings from both normotensive and hypertensive rats. R-and S-tetrahydrobiopterin (but not sepiapterin or dihydrobiopterin) potentiated the endothelium-dependent contractions to acetylcholine but only in aortas from hypertensive rats and in the presence of NG-nitro-L-arginine. In these aortas, the generation of oxygen-derived free radicals by the combination of xanthine plus xanthine oxidase also potentiated the endothelium-dependent contractions to acetylcholine. The presence of R-tetrahydrobiopterin did not alter the characteristics of the endothelium-dependent contractions because they were inhibited by valeryl salicylate, an inhibitor of cyclooxygenase-1, by S18886, a TP-receptor antagonist or by Tiron, a cell permeable superoxide anion scavenger. However, the contractions to acetylcholine, which are unaffected by the combination of superoxide dismutase and catalase, become significantly inhibited by these two scavengers in the presence of R-tetrahydrobiopterin. In the presence of NG-nitro-L-arginine, R-tetrahydrobiopterin did not affect the contractions to phenylephrine, U 46619, or to oxygen-derived free radicals generated by xanthine plus xanthine oxidase. These results indicate that the production of superoxide by the autoxidation of tetrahydrobiopterin selectively enhances endothelium-dependent contractions in the spontaneously hypertensive rat when nitric oxide synthase is inhibited.
tetrahydrobiopterin, nitric oxide, endothelium-dependent contractions, rats,, spontaneously hypertensive
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【期刊论文】Cardiac troponin T mutations in Chinese patients with hypertrophic cardiomyopathy
张寄南, Wu Heng-fang, Yang Di, WAN Wen-hui, BIAN Zhi-ping, XU Jin-dan, MA Wen-zhu, ZHANG Ji-nan
Chinese Medical Journal 2004; 117(6): 944-946,-0001,():
-1年11月30日
cardiomyopathy, hypertrophic, cardiac troponin T, mutation
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张寄南, Jj-Nan Zhang, James E.Wilks, and Joseph J.Billadello
The Journal of Biological Chemistry Vol. 270, No. 27, Issue of July 7, pp. 16134-16139, 1995,-0001,():
-1年11月30日
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【期刊论文】Trimetazidine improved Ca2+ handling in isoprenalinemediated myocardial injury of rats
张寄南, Dan Meng, Lin Feng, Xiang-Jian Chen, Di Yang and Ji-Nan Zhang
Exp Physiol 91.3 pp 591-601,-0001,():
-1年11月30日
Dysregulation of intracellular Ca2+ homeostasis plays an important role in mediating myocardial injury. We tested the hypothesis that treatment with trimetazidine (TMZ) would improve intracellular Ca2+ handling in myocardial injury of rats. The control group received saline only (10 ml kg-1 day-1, I.P.) for 7 days. In a second group, isoprenaline (ISO; 5 mg kg-1 day-1,S.C.) was administered to rats for 2 days to induce an acute injury of the myocardium. In a third group, treatment with TMZ (10 mg kg-1 day-1, I.P.) was initiated 1 day before ISO administration and continued for 7 days (n=7 rats in each group).Histopathological evaluation showed that TMZ prevented ISO-induced myocardial damage. TMZ preserved the ATP levels and decreased the maleic dialdehyde (MDA) content in the hearts compared with ISO-treated rats. The diastolic [Ca2+]I measured by loading with fura-2AM in isolated cardiomyocytes was increased significantly in ISO-treated rats compared to the control animals. TMZ prevented the rise of diastolic [Ca2+]I and the depression of caffeine-induced Ca2+ transients caused by ISO administration. The reduction in sarcoplasmic reticulum (SR) Ca2+ content in the heart cells and in cardiac SR Ca2+-ATPase activity in ISO-treated rats was abolished by TMZ, although there were no differences in SR Ca2+-ATPase protein levels between the control, ISO and ISO + 7 mz-treated rats. In addition, TMZ prevented the reduction in sarcolemmal L-type Ca2+ current density in the heart cells induced by ISO treatment. These results demonstrate that the treatment of rats with TMZ inhibited the increase of diastolic [Ca2+]I and prevented the decrease of SR Ca2+ content, SR Ca2+-ATPase activity and L-type Ca2+ current density in cardiomyocytes in ISO-mediatedmyocardial injury of rats. These changes inCa2+ handling could help to explain the favourable action of TMZ in myocardial injury.
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