Effects of angiotensin-converting enzyme and angiotensin II on hypoxia- induced proliferation of cultured intra-pulmonary artery smooth muscle cells

Tianzheng Yu, Chuan Tao Ma

Research output: Contribution to journalArticle

9 Citations (Scopus)

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 μm-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.

Original languageEnglish (US)
Pages (from-to)381-384
Number of pages4
JournalActa Pharmacologica Sinica
Volume21
Issue number4
StatePublished - May 4 2000

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Peptidyl-Dipeptidase A
Angiotensin II
Pulmonary Artery
Smooth Muscle Myocytes
Cell Hypoxia
Thymidine
Cell Count
Losartan
Captopril
Hypoxia
angiotensin-producing serum enzyme II
Cell Proliferation
Rabbits

Keywords

  • Angiotensin II
  • Angiotensin-converting enzyme
  • Cell hypoxia
  • Cultured cells
  • Pulmonary artery
  • Vascular smooth muscle

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Cite this

Effects of angiotensin-converting enzyme and angiotensin II on hypoxia- induced proliferation of cultured intra-pulmonary artery smooth muscle cells. / Yu, Tianzheng; Ma, Chuan Tao.

In: Acta Pharmacologica Sinica, Vol. 21, No. 4, 04.05.2000, p. 381-384.

Research output: Contribution to journalArticle

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N2 - 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 μm-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.

AB - 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 μm-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.

KW - Angiotensin II

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KW - Vascular smooth muscle

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