期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 280, 期 5, 页码 L870-L880出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.2001.280.5.L870
关键词
transient receptor potential gene; pulmonary hypertension; pulmonary artery smooth muscle cells
资金
- NHLBI NIH HHS [HL-54043, HL-64945] Funding Source: Medline
Agonist-induced increases in cytosolic Ca2+ concentration ([Ca2+](cyt)) in pulmonary artery (PA) smooth muscle cells (SMCs) consist of a transient Ca2+ release from intracellular stores followed by a sustained Ca2+ influx. Depletion of intracellular Ca2+ stores triggers capacitative Ca2+ entry (CCE), which contributes to the sustained increase in [Ca2+](cyt) and the refilling of Ca2+ into the stores. In isolated PAs superfused with Ca2+-free solution, phenylephrine induced a transient contraction, apparently by a rise in [Ca2+](cyt) due to Ca2+ release from the intracellular stores. The transient contraction lasted for 3-4 min until the Ca2+ store was depleted. Restoration of extracellular Ca2+ in the presence of phentolamine produced a contraction potentially due to a rise in [Ca2+](cyt) via CCE. The store-operated Ca2+ channel blocker Ni2+ reduced the store depletion-activated Ca2+ currents, decreased CCE, and inhibited the CCE-mediated contraction. In single PASMCs, we identified, using RT-PCR, five transient receptor potential gene transcripts. These results suggest that CCE, potentially through transient receptor potential-encoded Ca2+ channels, plays an important role in agonist-mediated PA contraction.
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