M. Gerova et al., LONG-TERM INHIBITION OF NO SYNTHASE INDUCES CARDIAC-HYPERTROPHY WITH A DECREASE IN ADRENERGIC-INNERVATION, Physiological Research, 45(4), 1996, pp. 339-344
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.