Morphometry of cardiomyocytes and capillary domains in the left ventricle myocardium was performed in control rats and in rats treated with nitro-L-arginine methyl ester 50 mg/kg/day p.o. for a period of 8 weeks. The myocardial hypertrophy accompanying the NO-deficient hypertension induced by chronic inhibition of NO synthase is characterized by an increase in thickness of myocardial fibres and by relative rarefaction of the capillary bed, e.g. an alteration in myocardial structure which is typical for pressure overload hypertrophy.