HYPOXIA AND ENDOTHELIN-1 STIMULATE DNA SYNTHESIS OF PULMONARY ARTERY SMOOTH MUSCLE CELLS
Chinese Medical Sciences JournalIssue 1, (1996)
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HYPOXIA AND ENDOTHELIN-1 STIMULATE DNA SYNTHESIS OF PULMONARY ARTERY SMOOTH MUSCLE CELLS
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CLC:R363
Published:1996
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[1]冯晓东,蔡英年.HYPOXIA AND ENDOTHELIN-1 STIMULATE DNA SYNTHESIS OF PULMONARY ARTERY SMOOTH MUSCLE CELLS[J].Chinese Medical Sciences Journal,1996(01):28-31.
HYPOXIA AND ENDOTHELIN-1 STIMULATE DNA SYNTHESIS OF PULMONARY ARTERY SMOOTH MUSCLE CELLS[J]. Chinese medical sciences journal, 1996, (1).
[1]冯晓东,蔡英年.HYPOXIA AND ENDOTHELIN-1 STIMULATE DNA SYNTHESIS OF PULMONARY ARTERY SMOOTH MUSCLE CELLS[J].Chinese Medical Sciences Journal,1996(01):28-31.DOI:
HYPOXIA AND ENDOTHELIN-1 STIMULATE DNA SYNTHESIS OF PULMONARY ARTERY SMOOTH MUSCLE CELLS[J]. Chinese medical sciences journal, 1996, (1).DOI:
HYPOXIA AND ENDOTHELIN-1 STIMULATE DNA SYNTHESIS OF PULMONARY ARTERY SMOOTH MUSCLE CELLS
Hypoxia and endothelin-1 (ET-1) are associated with constriction of pulmonary vasculature both in vivo and in vitro. However
the role of hypoxia and ET-1 in the vascular remodelling during the development of pulmonary hypertension is unclear. This study demonstrated that ET-1(0. 1 nmol/L to 100 nmol/L) increased the [ ̄3H]thymidine uptake in a dose-dependent manner in cultured bovine pulmonary artery smooth muscle cells(PASMC). which was enhanced by exposing PASMC to hypoxia (2%O2
93%N2
5%CO2 ). BQ123
the specific antagonist of endothelin receptor subtype A
eliminated the ET-1 medicated proliferation of PASMC and the cooperative effect of hypoxia. Some dilatory drugs could inhibite the mitogenic effect of ET-1. We also observed that hypoxia significantly increased [ ̄3H] thymidine uptake in PASMC without ET-1 and BQ123 could inhibite this effect. Radioimmunoassay suggested that there was an autocrine of ET-1 in cultured PASMC which was enhanced by hypoxia significantly.