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ASSA13-03-54 Adenosine A1 Agonist Inhibit the Hypertrophy of Cardiomyocyte Induced by Angiotensin II Through Calcineurin Pathway
  1. Tan Jian xin,
  2. Qian Dan dan,
  3. Lin Yongwen
  1. Pediatric department, the Affiliated Hospital of Guang Dong Medical College


Objective We aimed to study the mechanism and pathway of the adenosine A1 receptor agonist 2-chloro-N6 cyclopentyladenosine (CCPA) in the inhibition of the cardiomyocyte hypertrophy induced by angiotensin II (AngII) in vitro.

Methods Cardiomyocytes from neonatal SD rats were treated with AngII to generate a cardiomyocyte hypertrophy model. The cell cultures were randomised into four groups: (1) control; (2) AngII; (3) AngII + cyclosporin A (CsA); and (4) AngII + CCPA. The MTT method was used to measure cardiomyocyte viability. Protein synthesis was monitored by measuring the incorporation of tritiated leucine (3H-Leu), and the expression of β-myosin heavy chain (β-MHC) and calcineurin Aβ (CnAβ) mRNA was measured by semi-quantitative RT-PCR.

Results Forty-eight hours after AngII treatment, surface area, viability and 3H-Leu incorporation of the cardiomyocytes were significantly increased in a dose-dependent manner. Both CCPA and the calcineurin (CaN)-specific inhibitor CsA significantly inhibited AngII-induced cardiomyocyte 3H-Leu incorporation. These compounds also inhibited the mRNA expression of CnAβ and β-MHC in AngII-induced cardiomyocytes but had no significant effect on 3H-Leu incorporation in the control group. The inhibition by CCPA was dose-dependent within the range of 1 × 10–8 mol/L to 1 × 10–6 mol/L.

Conclusions The adenosine A1 receptor agonist CCPA can significantly inhibit AngII-induced cardiomyocyte hypertrophy in a manner related to the CaN signalling pathway.

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