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Objective To investigate the bradykinin (BK) , angiotensin - (1-7) [Ang-(1-7)] inhibit angiotensin Ⅱ (Ang Ⅱ) -induced cardiac fibroblasts (CFs) proliferation and collagen synthesis and its possible mechanism . Method the differential adhesion method cultured neonatal rat CFs, were randomly divided into five groups: control group (control group ) , Ang Ⅱ group , Ang -( 1-7 ) group , Ang Ⅱ Ang-(1-7) and Ang Ⅱ Ang-(1-7) HOE-140 group . MTT reflect cell proliferation , hydroxyproline reflects collagen synthesis by nitrate reductase method for the determination of the content of NO and cGMP content was measured by radioimmunoassay . Results (1) than the control group of Ang Ⅱ 10 -7 M cells were incubated for 36h can be significantly induced CFs number increased and collagen synthesis [100 % vs ( 51.8 ± 1.8 ) % , 100 % vs. (62.2 ± 3.1)% P lt; 0.01]. (2) Ang-(1-7) in a concentration -dependent inhibition of Ang II -induced CFs number increased , and the inhibition of collagen synthesis , and its Ang-(1-7) 10 -6 M cells can The decline in the number of collagen content decreased to (57.9 ± 2.1)%, ( 72.1 ± 2.3 ) % ( P lt; 0.01 ) . (3) compared with the control group , Ang II group NO and cGMP content significantly lower (P lt; 0.01), while Ang - (1-7) 10 -6 < / sup > M can be significantly increased NO and cGMP content , with Ang Ⅱ group , rose to ( 177.2 ± 6.9 ) % , ( 242.3 ± 19.1 ) % ( P lt; 0.01 ) . (4) bradykinin B 2 receptor blocker HOE- 140 10 -8 < / sup > M significantly reduced the Ang-(1-7) inhibit CFs proliferation and collagen synthesis and to promote the CFs the release of NO and cGMP , by Ang Ⅱ Ang - (1-7) group and Ang Ⅱ Ang-(1-7) HOE-140 group than ( 57.9 ± 2.1 ) % , ( 72.1 ± 2.3 ) % , ( 177.2 ± 6.9) % , ( 242.3 ± 19.1 ) % , respectively, into (88.9 ± 4.2 ) % , ( 87.8 ± 1.2 ) % , ( 125.7 ± 8.2) % , ( 162.2 ± 14.7 ) % ( P lt; 0.01 ) . Conclusion Ang - ( 1-7 ) may promote the production of NO and cGMP interaction with BK , thereby inhibiting the Ang II -induced CFs proliferation and collagen synthesis .
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