期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 288, 期 6, 页码 L1049-L1058出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00379.2004
关键词
voltage-gated K+
资金
- NHLBI NIH HHS [HL-67191, HL-67919, HL-51912] Funding Source: Medline
In pulmonary arterial smooth muscle cells (PASMCs), voltage-gated K+ ( K-v) channels play an important role in regulating membrane potential, cytoplasmic free Ca2+ concentration, and pulmonary vasomotor tone. Previous studies demonstrated that exposure of rats to chronic hypoxia decreased Kv channel function in PASMCs from distal pulmonary arteries (dPA). To determine whether this decrease in function was due to decreased expression of Kv channel proteins and which Kv proteins might be involved, we analyzed Kv channel gene expression in intact, endothelium-denuded dPAs obtained from rats exposed to 10% O-2 for 3 wk. K(v)1.1, K(v)1.2, K(v)1.4, K(v)1.5, K(v)1.6, K(v)2.1, K(v)3.1, K(v)4.3, and K(v)9.3 channel alpha- subunits and K(v)1, K(v)2, and K(v)3 beta- subunits were expressed in rat dPAs. Exposure to chronic hypoxia decreased mRNA and protein levels of K(v)1.1, K(v)1.5, K(v)1.6, K(v)2.1, and K(v)4.3 alpha-subunits in dPAs but did not alter gene or protein expression of these channels in aorta. Furthermore, chronic hypoxia did not alter the mRNA levels of alpha-subunits in dPAs. These results suggest that diminished transcription of Kv alpha-subunits may reduce the number of functional Kv channels in dPAs during prolonged hypoxia, causing the decreased Kv current previously observed in PASMCs and leading to pulmonary artery vasoconstriction.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据