Adrenomedullin may provide a compensatory mechanism to attenuate left ventricular hypertrophy (LVH). NOS inhibition, induced by chronic administration of N-nitro-L-arginine-methyl-ester (L-NAME) to rats, induces cardiac hypertrophy in some, but not all cases; there are few reports of direct assessment of cardiomyocyte parameters. The objective was to characterize hypertrophic parameters in left (LV) and right ventricular (RV) cardiomyocytes, following administration of L-NAME to rats for 8 weeks and to determine whether adrenomedullin and its receptor components were up-regulated. Following treatment with L-NAME (20 and 50mg/kg/day), compared to non-treated animals: (1) systolic blood pressure increased (by 34.2 and 104.9 mmHg); (2) heart weight: body weight ratio increased 24.1% at the higher dose (P<0.05); (3) cardiomyocyte protein mass increased (p= ns) (by 22.4% in LV, and 59.0% RV at the higher dose); (4) cardiomyocyte protein synthesis (¹⁴C-phenylalanine incorporation) increased (P<0.05) (by 93% and 66% in LV; by 137% and 137% in RV at 20 and 50mg/kg/day, respectively); (5) expression of sk -actin (3.3 and 2.6 fold), ANP (1.2 and 17.9 fold) , BNP (2.9 and 3.1 fold) and endothelin-1 (2.7 and 3.9 fold) mRNAs was enhanced (P<0.05) in LV but not RV cardiomyocytes at 20 and 50 mg/kg/day, respectively; (6) expression of adrenomedullin (1.8 fold), RAMP3 (3.1 fold) and RAMP2 (1.8 fold), (but not CL and RAMP1) mRNAs was increased by L-NAME (20mg/kg/day) in LV. In conclusion, L-NAME enhanced protein synthesis in both LV and RV cardiomyocytes but elicited a hypertrophic phenotype accompanied by altered expression of the counter-regulatory peptide, adrenomedullin, and receptor components (RAMP2, RAMP3) in LV only, indicating that the former is due to impaired NO synthesis, while the phenotypic changes are due to pressure overload.