T Z Yu1, C T Ma. 1. Laboratory of Cardiovascular Physiology, Hunan Medical University, Changsha 410078, China. tianzheng_yu@163.net
Abstract
AIM: To investigate whether local angiotensin-converting enzyme (ACE) and endogenous angiotensin II (ANG II) are involved directly in the proliferation of intra-pulmonary artery smooth muscle cells (PASMC) induced by hypoxia. METHODS: Smooth muscle cells isolated from rabbit intra-pulmonary artery (300-400 microns-diameter) were cultured and used in the 3-8 passages. [3H]Thymidine incorporation and cell counts were used to measure PASMC proliferation. RESULTS: Exposure of PASMC to hypoxia for 24 h resulted in an increase in the [3H]thymidine incorporation and cell number by 166.6% and 52.0% as compared with normoxia (P < 0.01). Treatment with either captopril or losartan markedly inhibited the increase, compared with the control, [3H]thymidine incorporation was inhibited by 51.3% (P < 0.01) and 49.8% (P < 0.01) and cell number was inhibited by 22.2% (P < 0.01) and 17.9% (P < 0.01), respectively, while PD-123319 showed no significant effect. CONCLUSION: Local overexpression of PASMC ACE and ANG II play an important role in the proliferation of PASMC induced by hypoxia.
AIM: To investigate whether local angiotensin-converting enzyme (ACE) and endogenous angiotensin II (ANG II) are involved directly in the proliferation of intra-pulmonary artery smooth muscle cells (PASMC) induced by hypoxia. METHODS: Smooth muscle cells isolated from rabbit intra-pulmonary artery (300-400 microns-diameter) were cultured and used in the 3-8 passages. [3H]Thymidine incorporation and cell counts were used to measure PASMC proliferation. RESULTS: Exposure of PASMC to hypoxia for 24 h resulted in an increase in the [3H]thymidine incorporation and cell number by 166.6% and 52.0% as compared with normoxia (P < 0.01). Treatment with either captopril or losartan markedly inhibited the increase, compared with the control, [3H]thymidine incorporation was inhibited by 51.3% (P < 0.01) and 49.8% (P < 0.01) and cell number was inhibited by 22.2% (P < 0.01) and 17.9% (P < 0.01), respectively, while PD-123319 showed no significant effect. CONCLUSION: Local overexpression of PASMCACE and ANG II play an important role in the proliferation of PASMC induced by hypoxia.