Journal of Capital Medical University ›› 2009, Vol. 30 ›› Issue (2): 167-171.

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Role of Transient Potential Vanilloid Receptor 1 Channels in Hypoxia-induced Cytosolic Ca2+ Increase of Human Pulmonary Arterial Smooth Muscle Cells

WANG Yue-xiu1,2,3, WANG Chen1,3, WANG Cong1,2,3, LIU Jie2,3, WANG Jun2,3   

  1. 1. Department of Respiratory Diseases, Beijing Chaoyang Hospital, Capital Medical University, Beijing Institute of Respiratory Medicine;2. Department of Physiology, School of Basic Medical Sciences, Capital Medical University;3. Department of Respiratory Diseases, Capital Medical University
  • Received:2008-12-18 Revised:1900-01-01 Online:2009-04-21 Published:2009-04-21

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Abstract:

Objective To investigate the role of transient potential vanilloid receptor 1(TRPV1) channels on cytosolic Ca2+ concentration(340 nm/380 nm ratio of the fluorescence image) of hypoxic human pulmonary artery smooth muscle cells(HPASMCs) and its possible signal pathway. Methods 4',6-diamidino-2-phenylindole(DAPI) staining and flow cytometry were used to detect the proliferation of HPASMCs under normoxia or hypoxia (3％O2, 72 h) conditions. Cytosolic Ca2+ concentration(［Ca2+］cyt) was measured with a dynamic digital imaging system. Results The capability of HPASMCs proliferation significantly increased under hypoxic condition. Capsazepine(a TRPV1 channel inhibitor) could inhibit the HPASMCs proliferation. Hypoxia markedly increased resting cytosolic Ca2+ concentration and enhanced cyclopiazonic acid-induced capacitative Ca2+ entry(CCE) in HPASMCs. Capsazepine(10 μM) decreased CCE under hypoxia condition, but there was no effect on normoxia cultured group. Conclusion These results suggest that TRPV1 may be a critical pathway or mediator in hypoxia-induced increase of cytosolic Ca2+ concentration, CCE and the proliferation of HPASMCs.

Key words: pulmonary arterial smooth muscle cells, transient potential vanilloid receptor 1, store-operated calcium channels

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