2004PubMedRequires access

[Effects of iptakalim on the proliferation of cultured rabbit pulmonary arterial smooth muscle cells induced by endothelin-1].

Xie Wp, Hong Wang, Qi Xie, Hongxing Shen, Hai Wang, Gang Hu

Open publisher page 0 citations

Abstract

OBJECTIVE: To explore the effects of iptakalim on the proliferation of rabbit pulmonary arterial smooth muscle cell(PASMC) induced by endothelin-1(ET-1) in vitro. METHODS: The experimental models of proliferation of rabbit PASMC induced by ET-1 in vitro were established and [(3)H]-thymidine ([(3)H]-TdR) incorporation and flow cytometric analysis(FCA) were used. RESULTS: The value of [(3)H]-TdR incorporation in ET-1 group was increased 1.468 times higher than that in control group. Iptakalim at the concentrations of 10(-7) mol/L, 10(-6) mol/L, 10(-5) mol/L lowered [(3)H]-TdR incorporation by (19.8 +/- 4.6)%,(41.2 +/- 9.5)%, (54.7 +/- 10.1)%, declined the total of the DNA synthesis (S) and the mitotic phase (G(2)/M) ratios by (36.6 +/- 5.7)%, (42.6 +/- 4.9)%, (66.3 +/- 4.7)%, and increased the static phase (G(0)/G(1)) ratio by (14.4 +/- 3.0)%, (17.9 +/- 2.6)%, (27.9 +/- 3.2)%, respectively, compared with the value of the cells treated with ET-1 only (P < 0.01). Glibenclimide abolished the effect of iptakalim on [(3)H]-TdR incorporation. CONCLUSION: Iptakalim has an inhibitory effect on PASMC proliferation induced by ET-1 through activating ATP sensitive potassium (K(ATP)) channels.

About this research paper

What this paper is about

OBJECTIVE: To explore the effects of iptakalim on the proliferation of rabbit pulmonary arterial smooth muscle cell(PASMC) induced by endothelin-1(ET-1) in vitro. METHODS: The experimental models of proliferation of rabbit PASMC induced by ET-1 in vitro were established and [(3)H]-thymidine ([(3)H]-TdR) incorporation and flow cytometric analysis(FCA) were used. RESULTS: The value of [(3)H]-TdR incorporation in ET-1 group was increased 1.468 times higher than that in control group. Iptakalim at the concentrations of 10(-7) mol/L, 10(-6) mol/L, 10(-5) mol/L lowered [(3)H]-TdR incorporation by (19.8 +/- 4.6)%,(41.2 +/- 9.5)%, (54.7 +/- 10.1)%, declined the total of the DNA synthesis (S) and the mitotic phase (G(2)/M) ratios by (36.6 +/- 5.7)%, (42.6 +/- 4.9)%, (66.3 +/- 4.7)%, and increased the static phase (G(0)/G(1)) ratio by (14.4 +/- 3.0)%, (17.9 +/- 2.6)%, (27.9 +/- 3.2)%, respectively, compared with the value of the cells treated with ET-1 only (P < 0.01). Glibenclimide abolished the effect of iptakalim on [(3)H]-TdR incorporation. CONCLUSION: Iptakalim has an inhibitory effect on PASMC proliferation induced by ET-1 through activating ATP sensitive potassium (K(ATP)) channels.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

OBJECTIVE: To explore the effects of iptakalim on the proliferation of rabbit pulmonary arterial smooth muscle cell(PASMC) induced by endothelin-1(ET-1) in vitro. METHODS: The experimental models of proliferation of rabbit PASMC induced by ET-1 in vitro were established and [(3)H]-thymidine ([(3)H]-TdR) incorporation and flow cytometric analysis(FCA) were used. RESULTS: The value of [(3)H]-TdR incorporation in ET-1 group was increased 1.468 times higher than that in control group. Iptakalim at the concentrations of 10(-7) mol/L, 10(-6) mol/L, 10(-5) mol/L lowered [(3)H]-TdR incorporation by (19.8 +/- 4.6)%,(41.2 +/- 9.5)%, (54.7 +/- 10.1)%, declined the total of the DNA synthesis (S) and the mitotic phase (G(2)/M) ratios by (36.6 +/- 5.7)%, (42.6 +/- 4.9)%, (66.3 +/- 4.7)%, and increased the static phase (G(0)/G(1)) ratio by (14.4 +/- 3.0)%, (17.9 +/- 2.6)%, (27.9 +/- 3.2)%, respectively, compared with the value of the cells treated with ET-1 only (P < 0.01). Glibenclimide abolished the effect of iptakalim on [(3)H]-TdR incorporation. CONCLUSION: Iptakalim has an inhibitory effect on PASMC proliferation induced by ET-1 through activating ATP sensitive potassium (K(ATP)) channels.

Key concepts: Endothelin 1, Chemistry, In vitro, Cell growth, Smooth muscle, Molecular biology, Rabbit (cipher), DNA synthesis

Related papers

Back to paper searchBrowse research topicsOriginal source
[Effects of iptakalim on the proliferation of cultured rabbit pulmonary arterial smooth muscle cells induced by endothelin-1]. — Research Paper | ScholarLens