Geng Bin, Yan Hui, Zhong Guang-Zhen, Zhang Chun-Yu, Chen Xiao-Bo, Jiang Hong-Feng, Tang Chao-Shu, Du Jun-Bao
Department of Physiology, Peking University School of Basic Medical Sciences, Beijing, China.
Beijing Da Xue Xue Bao Yi Xue Ban. 2004 Feb;36(1):106.
Hydrogen sulfide (H(2)S) may be endogenously produced by cystathionine beta-lyase (CBS) and cystathionine gamma-lyase (CSE) as a cardiovascular physiological functional factor. On the hypoxic pulmonary hypertension (HPH) animal model, the plasma H(2)S concentration, the gene expression and the activity (CSE) were decreased in lung tissues In L-NAME induced hypertension and spontaneous hypertension rats (SHR) models, the plasma H(2)S concentration, vascular CSE activity and mRNA expression were obviously decreased. When H(2)S was exogenously supplied, systolic pressure obviously decrease. These studies suggested that CSE/H(2)S pathway participated in the pathophysiological development of hypertension. The endogenous level of H(2)S produced by some arterial tissues increased in both septic and endotoxic shock rats. The level of H(2)S highly correlated with the endogenous level of NO. These results suggest that H(2)S may be a novel cardiovascular functional regulator.
硫化氢(H₂S)可能作为一种心血管生理功能因子由胱硫醚β-裂解酶(CBS)和胱硫醚γ-裂解酶(CSE)内源性产生。在缺氧性肺动脉高压(HPH)动物模型中,肺组织中的血浆H₂S浓度、基因表达及活性(CSE)均降低。在L-精氨酸甲酯(L-NAME)诱导的高血压大鼠和自发性高血压大鼠(SHR)模型中,血浆H₂S浓度、血管CSE活性及mRNA表达均明显降低。当外源性给予H₂S时,收缩压明显下降。这些研究提示CSE/H₂S途径参与了高血压的病理生理发展过程。在脓毒症和内毒素休克大鼠中,一些动脉组织产生的H₂S内源性水平均升高。H₂S水平与内源性一氧化氮(NO)水平高度相关。这些结果提示H₂S可能是一种新型的心血管功能调节因子。