Imbalance of endogenous homocysteine and hydrogen sulfide metabolic pathway in essential hypertensiv

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Background Hypertension is a common disease of the cardiovascular system.So far,the pathogenesis of primaryhypertension remains unclear.The elaboration of its pathogenesis is an important topic in the field which calls for urgentresolution.The aim of this study was to probe into the metabolic imbalance of homocysteine (Hcy) and hydrogen sulfide(H2S) in children with essential hypertension,and its significance in the pathogenesis of essential hypertension.Methods Twenty-five children with essential hypertension and 30 healthy children with normal blood pressure wereenrolled in the study.The medical history was investigated and a physical examination was conducted on the subjects.Plasma Hcy content was examined by fluorescence polarization immunoassay (FPIA).The plasma H_2S level wasdetected by a modified method with a sulfide electrode.Data were presented as mean+standard deviation.The t testwas applied to the mean values of both groups.Pearson linear correlation analysis was applied to the plasma Hcy andH2S as well as to the systolic pressure against the plasma H_2S/Hcy ratio.Results Plasma Hcy,an intermittent metabolite Of the endogenous methionine pathway,was markedly increased butplasma H_2S,a final product of this pathway was significantly decreased in hypertensive cases when compared withnormal subjects ((Hcy:(12.68±9.69) μmol/L vs (6.62±4.79) μmol/L (t=2.996,P<0.01);H_2S:(51.93±6.01) μmol/L vs(65.70±5.50) μmol/L) (t=-8.670,P<0.01)).The ratio of plasma H_2S/Hcy in children with hypertension was 5.83±2.91,while that of the control group was 11.60±3.30,and the difference is significant with a t=-6.610 and P<0.01.A negativecorrelation existed between plasma Hcy and H_2S concentrations,r=-0.379,P<0.05.And a negative correlation wasfound between systolic blood pressure and the plasma H_2S/Hcy ratio,r=-0.687,P<0.05.Conclusion There was a metabolic imbalance of homocysteine and hydrogen sulfide in essential hypertensivechildren.Chin Med J 2007;120(5):389-393 Background Hypertension is a common disease of the cardiovascular system. So far, the pathogenesis of primary hyperthyroidism remains unclear. The elaboration of its pathogenesis is an important topic in the field which calls for urgent resolution. The AIM of this study was to probe into the metabolic imbalance of homocysteine ​​(Hcy) and hydrogen sulfide (H2S) in children with essential hypertension, and its significance in the pathogenesis of essential hypertension. Methods Twenty-five children with essential hypertension and 30 healthy children with normal blood pressure were enrolled in the study. medical history was investigated and a physical examination was conducted on the subjects.Plasma Hcy content was examined by fluorescence polarization immunoassay (FPIA). The plasma H_2S level wasdetected by a modified method with a sulfide electrode. Data were presented as mean + standard deviation.The t testwas applied to the mean values ​​of both groups. Pearson linear correlation analysis was applied to the plasma Hcy and H2S as well as to the systolic pressure against the plasma H_2S / Hcy ratio. Results Plasma Hcy, an intermittent metabolite Of the endogenous methionine pathway, was markedly increased butplasma H_2S, a final product of this pathway was significantly less in hypertensive cases (51.93 ± 6.01) μmol / L vs (65.70 ± 5.50), compared with normal subjects (Hcy: (12.68 ± 9.69) μmol / L vs 6.62 ± 4.79 μmol / L ) μmol / L) (t = -8.670, P <0.01). The ratio of plasma H_2S / Hcy in children with hypertension was 5.83 ± 2.91, while that of the control group was 11.60 ± 3.30, and the difference was significant with at = -6.610 and P <0.01.A negativecorrelation existed between plasma Hcy and H 2 S concentrations, r = -0.379, P <0.05.And a negative correlation was found between systolic blood pressure and the plasma H_2S / Hcy ratio, r = -0.687, P <0.05.Conclusion There was a metabolic imbalance of homocysteine ​​and hydrogen sulfide in essential hypertensive children. Chin Med J 2007; 120 (5): 389-393
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