Background Hypertension is a common disease of the cardiovascular system. So far, the pathogenesis of primary hypertension 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. 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 H2S level was detected by a modified method with a sulfide electrode. Data were presented as mean＋standard deviation. The t test was 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 H2S/Hcy ratio. Results Plasma Hcy, an intermittent metabolite of the endogenous methionine pathway, was markedly increased but plasma H2S, a final product of this pathway was significantly decreased in hypertensive cases when compared with normal subjects （（Hcy： （12.68±9.69） μmol/L vs （6.62±4.79） μmol/L （t=2.996, ,P〈0.01）; H2S： （51.93±6.01） μ/L vs （65.70±5.50） μmol/L） （t=-8.670, ,P〈0.01））. The ratio of plasma H2S/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 negative correlation existed between plasma Hcy and H2S concentrations, r=-0.379, P〈0.05. And a negative correlation was found between systolic blood pressure and the plasma H2S/Hcy ratio, r=-0.687, P〈0.05. Conclusion There was a metabolic imbalance of homocysteine and hydrogen sulfide in essential hy
目的 探讨新型气体信号分子二氧化硫（SO2）对自发性高血压大鼠（SHR）主动脉平滑肌细胞增殖与凋亡的调节作用。方法 4周龄SHR大鼠随机分为SHR对照组、Na2SO3／NaHSO3组（外源性SO2供体组），每组8只。4周龄正常血压WistarKyoto（WKY）大鼠8只作为正常对照（WKY对照组）。5周后检测大鼠血压及主动脉形态学指标，以高效液相色谱（HPLC）法测定血浆SO2水平；采用原位缺口末端标记方法（TUNEL）检测大鼠主动脉平滑肌细胞凋亡；采用免疫组织化学方法检测主动脉平滑肌细胞增殖细胞核抗原（PCNA）及凋亡相关蛋白Bcl-2、Fas和半胱氨酸蛋白水解酶（caspase）-3的表达，并进行图像分析。结果 5周后SHR对照组血压、血管壁厚与内径比均明显高于WKY对照组[（172±10）nl／nHgV8（112±9）nl／nHg、0．073±0．004V80．057±0．004，均P〈0．01，1mm Hg=0．133kPa]，血浆SO2水平显著低于WKY对照组[（6．4±1．5）μmol／LV8（11．3±1．0）μmol／L]，主动脉平滑肌细胞增殖指数高（0．32±0．06 vs 0．05±0．03），而凋亡指数小（0．16±0．07 vs 0．30±0．19），主动脉平滑肌细胞Bcl-2蛋白表达高（0．209±0．007 vs 0．202±0．006，P〈0．01），Fas、caspase-3蛋白表达弱（0．205±0．006 vs 0．211±0．005、0．229±0．005 vs 0．244±0．010，均P〈0．01）。外源性SO2供体组与SHR对照组比较，血压低[（128±7）mm Hg]，血管壁厚与内径比低（0．066±0．002），血浆SO2含量高[（8．3±1．0）μmol／L]，主动脉平滑肌细胞增殖指数低（0．14±0．03），凋亡指数高（0．40±0．11），主动脉平滑肌细Bcl-2蛋白表达低（0．199±0．006），Fas和caspase-3蛋白呈高表达（分别为0．218±0．003、0．251±0．011，均P〈0．01）。结论 SO2可抑制高血压大鼠主动脉血管平滑肌细胞增殖、促进其细胞凋亡。SO2促进细胞凋亡的途径可能与其对主动脉平滑肌细�
