2007Chinese Journal of Cardiovascular ReviewRequires access

The role of angiotensinIin the proliferation of vascular smooth muscle cells induced by angiotensin II

Nana Zhang

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Abstract

Objective To explore the effect of angiotensin-(1-7) Ang-(1-7) on the proliferation of vascular smooth muscle cells (VSMCs) induced by angiotensin Ⅱ(AngⅡ). Methods The primary culture of VSMCs was performed using tissue explant method. Cells at passage 3 to 5 were used for experiment and were randomly divided into control group,AngⅡ group, Ang-(1-7) group, AngⅡ+ Ang-(1-7) group and AngⅡ+ Ang-(1-7)+(A-779) group. The synthesis of DNA was measured by incorporation of 3H -thymidine (3H-TdR) and the proliferation of VSMCs was measured by crystal violet staining. Results ⑴Compared with the control, 3H-TdR incorporation was significantly increased after incubating the VSMCs with 100 nmol/L AngⅡ for 24 hours. However 1000 nmol/L Ang-(1-7) decreaced the 3H-TdR incorporation. ⑵ Compared with the AngⅡ control, Ang-(1-7) with (10 nmol/L,100 nmol/L,1000 nmol/L) does-dependently inhibited proliferation of VSMCs with no cytotoxic effect. The effect of Ang-(1-7) could be blocked by its specific receptor blocker A-779. ⑶The crystal violet staining result show that AngⅡ increased the cell number(P0.05),and Ang-(1-7) inhibited the increase of cell number induced by AngⅡ.Conclusion Ang-(1-7) could inhibit the proliferation of cultured rat's VSMCs induced by AngⅡ via its specific receptor.

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Objective To explore the effect of angiotensin-(1-7) Ang-(1-7) on the proliferation of vascular smooth muscle cells (VSMCs) induced by angiotensin Ⅱ(AngⅡ). Methods The primary culture of VSMCs was performed using tissue explant method. Cells at passage 3 to 5 were used for experiment and were randomly divided into control group,AngⅡ group, Ang-(1-7) group, AngⅡ+ Ang-(1-7) group and AngⅡ+ Ang-(1-7)+(A-779) group. The synthesis of DNA was measured by incorporation of 3H -thymidine (3H-TdR) and the proliferation of VSMCs was measured by crystal violet staining. Results ⑴Compared with the control, 3H-TdR incorporation was significantly increased after incubating the VSMCs with 100 nmol/L AngⅡ for 24 hours. However 1000 nmol/L Ang-(1-7) decreaced the 3H-TdR incorporation. ⑵ Compared with the AngⅡ control, Ang-(1-7) with (10 nmol/L,100 nmol/L,1000 nmol/L) does-dependently inhibited proliferation of VSMCs with no cytotoxic effect. The effect of Ang-(1-7) could be blocked by its specific receptor blocker A-779. ⑶The crystal violet staining result show that AngⅡ increased the cell number(P0.05),and Ang-(1-7) inhibited the increase of cell number induced by AngⅡ.Conclusion Ang-(1-7) could inhibit the proliferation of cultured rat's VSMCs induced by AngⅡ via its specific receptor.

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Available abstract

Objective To explore the effect of angiotensin-(1-7) Ang-(1-7) on the proliferation of vascular smooth muscle cells (VSMCs) induced by angiotensin Ⅱ(AngⅡ). Methods The primary culture of VSMCs was performed using tissue explant method. Cells at passage 3 to 5 were used for experiment and were randomly divided into control group,AngⅡ group, Ang-(1-7) group, AngⅡ+ Ang-(1-7) group and AngⅡ+ Ang-(1-7)+(A-779) group. The synthesis of DNA was measured by incorporation of 3H -thymidine (3H-TdR) and the proliferation of VSMCs was measured by crystal violet staining. Results ⑴Compared with the control, 3H-TdR incorporation was significantly increased after incubating the VSMCs with 100 nmol/L AngⅡ for 24 hours. However 1000 nmol/L Ang-(1-7) decreaced the 3H-TdR incorporation. ⑵ Compared with the AngⅡ control, Ang-(1-7) with (10 nmol/L,100 nmol/L,1000 nmol/L) does-dependently inhibited proliferation of VSMCs with no cytotoxic effect. The effect of Ang-(1-7) could be blocked by its specific receptor blocker A-779. ⑶The crystal violet staining result show that AngⅡ increased the cell number(P0.05),and Ang-(1-7) inhibited the increase of cell number induced by AngⅡ.Conclusion Ang-(1-7) could inhibit the proliferation of cultured rat's VSMCs induced by AngⅡ via its specific receptor.

Key concepts: Vascular smooth muscle, Angiotensin II, Endocrinology, Internal medicine, DNA synthesis, Receptor, Renin–angiotensin system, Cell growth

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