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.