摘要
Hydrogen sulfide (H 2S) may be endogenously produced by cystathionine β lyase (CBS) and cystathionine γ lyase (CSE) as a cardiovascular physiological functional factor. On the hypoxic pulmonary hypertension (HPH) animal model, the plasma H 2S 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 2S concentration, vascular CSE activity and mRNA expression were obviously decreased. When H 2S was exogenously supplied, systolic pressure obviously decrease. These studies suggested that CSE/H 2S pathway participated in the pathophysiological development of hypertension. The endogenous level of H 2S produced by some arterial tissues increased in both septic and endotoxic shock rats. The level of H 2S highly correlated with the endogenous level of NO These results suggest that H 2S may be a novel cardiovascular functional regulator.
Hydrogen sulfide (H 2S) may be endogenously produced by cystathionine β lyase (CBS) and cystathionine γ lyase (CSE) as a cardiovascular physiological functional factor. On the hypoxic pulmonary hypertension (HPH) animal model, the plasma H 2S 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 2S concentration, vascular CSE activity and mRNA expression were obviously decreased. When H 2S was exogenously supplied, systolic pressure obviously decrease. These studies suggested that CSE/H 2S pathway participated in the pathophysiological development of hypertension. The endogenous level of H 2S produced by some arterial tissues increased in both septic and endotoxic shock rats. The level of H 2S highly correlated with the endogenous level of NO These results suggest that H 2S may be a novel cardiovascular functional regulator.
出处
《北京大学学报(医学版)》
CAS
CSCD
北大核心
2004年第1期106-106,共1页
Journal of Peking University:Health Sciences
基金
国家重点基础研究发展规划项目基金 (G2 0 0 0 0 5 690 5 )
国家自然科学基金 ( 3 0 2 713 73 )资助~~