ABSTRACT
Aim To demonstrate the effects and mechanism of adenosine A1 receptor agonist R(-)-N6-(2-phenylisopropyl) adenosine(R-PIA) on high glucose(HG)-induced myocardial hypertrophy by in vitro cultured myocardial cells from neonatal rats.Methods The protein content was assayed by the method of Lowry. The expression of p-ERK1/2 and ERK1/2 was determined by Western blot.The [Ca~(2+)]I transient changes of cell loaded Fura-2/AM were measured by Till image system.Results 1 μmol·L~(-1) R-PIA and U0126 inhibited similarly HG-induced increase of the protein content and [Ca~(2+)]I transient along with the relative expression of p-ERK1/2.These responses were completely abolished by adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine(CPDPX).Conclusion Adenosine A1 receptor stimulation significantly inhibits HG-induced myocardial hypertrophy by mediating ERK1/2 pathway and Ca~(2+).
ABSTRACT
Objective To demonstrate the inhibitory effect of adenosine A_1 receptor agonist R(-)-N6-(2-phe- nylisopropyl) adenosine (R-HA) and cross-talk between adenosine A_1 receptor and CaMKII on Isoproterenol (Iso)- induced hypertrophy in cultured myocardial cells in neonatal rats.Methods The protein synthesis was determined by incorporation of [~3H]-leucine into myocyte protein.The expression of CaMK Ⅱ ? B was determined by Western- blot.The [Ca~(2+)]i transient was measured in myocytes loaded with fura-2 by the spectrofluorometric method. Results R-PIA (1?mol/L) inhibited Iso(10 ?mol/L)-induced increase of [~3 H-]-leucine incorporation [(R-PIA: 974.8?58.6) vs (Iso:1220.8?240.5) count per min per well,P