LONG-TERM INHIBITION OF NO SYNTHASE INDUCES CARDIAC-HYPERTROPHY WITH A DECREASE IN ADRENERGIC-INNERVATION

Data concerning the effect of NO on the function and structure of the heart are controversial We have studied two main questions (i) Does th e heart muscle reflect the hypertension induced by long-term inhibitio n of NO synthase? (ii) Since the arginine-NO pathway is also operative in the autonomic nervous system, the second goal was to ascertain the possible changes of the adrenergic nervous system in the heart after long-term NO synthase inhibition. Wistar rats were administered L-NAME in drinking water (50 mg/kg bw/day) for 8 weeks Systolic blood pressu re and heart rate were monitored weekly. The heart/body weight ratio w ere determined at the end of experiment. The adrenergic nerve terminal s visualized by histochemistry were counted according to Haug's point counting method. Blood pressure increased significantly in L-NAME-trea ted rats No changes were found in the heart rate. Heart/body weight ra tio increased markedly. Surprisingly, the density of adrenergic nerve terminals did not alter accordingly. The density of adrenergic nerve t erminals in the left ventricle and septum decreased but no significant changes were found in the left atrium and the right ventricle. Hypert ension due to NO deficiency induced cardiac hypertrophy that was chara cterized by a decline in the density of adrenergic innervation of the overloaded left ventricle and septum.