title: Long-term inhibition of NO synthase induces cardiac hypertrophy with a decrease in adrenergic innervation.
abstract: Data concerning the effect of NO on the function and structure of the heart are controversial. We have studied two main questions: (i) Does the heart muscle reflect the hypertension induced by long-term inhibition 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 pressure and heart rate were monitored weekly. The heart/body weight ratio were determined at the end of experiment. The adrenergic nerve terminals visualized by histochemistry were counted according to Haug's point counting method. Blood pressure increased significantly in L-NAME-treated rats. No changes were found in the heart rate. Heart/body weight ratio increased markedly. Surprisingly, the density of adrenergic nerve terminals did not alter accordingly. The density of adrenergic nerve terminals in the left ventricle and septum decreased but no significant changes were found in the left atrium and the right ventricle. Hypertension due to NO deficiency induced cardiac hypertrophy that was characterized by a decline in the density of adrenergic innervation of the overloaded left ventricle and septum.
authors.affiliation: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
authors.forename: M
authors.initials: M
authors.lastname: Gerová
authors.forename: B
authors.initials: B
authors.lastname: Hartmannová
authors.forename: S
authors.initials: S
authors.lastname: Dolezel
authors.forename: L
authors.initials: L
authors.lastname: Jezek
mesh_terms: D000320:Adrenergic Fibers / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D004791:Enzyme Inhibitors; D006321:Heart / Q000294:innervation*; D006339:Heart Rate; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced / Q000201:enzymology* / Q000503:physiopathology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D009929:Organ Size; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester