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Long-term inhibition of NO synthase induces cardiac hypertrophy with a decrease in adrenergic innervation

M Gerová1, B Hartmannová, S Dolezel

  • 1Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic.

Physiological Research
|January 1, 1996
PubMed
Summary
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Long-term inhibition of nitric oxide (NO) synthase in rats caused hypertension and cardiac hypertrophy. Adrenergic nerve terminal density decreased in the overloaded left ventricle and septum, indicating structural changes in cardiac innervation.

Area of Science:

  • Cardiovascular Physiology
  • Neurocardiology
  • Pharmacology

Background:

  • Nitric oxide (NO) plays a complex role in cardiovascular function.
  • The arginine-NO pathway is involved in both cardiac function and autonomic nervous system regulation.
  • Previous data on NO's cardiac effects are conflicting, necessitating further investigation.

Purpose of the Study:

  • To investigate the impact of long-term nitric oxide synthase (NOS) inhibition on cardiac structure and function.
  • To determine if hypertension induced by NOS inhibition affects cardiac muscle.
  • To assess changes in cardiac adrenergic nervous system following chronic NOS inhibition.

Main Methods:

  • Wistar rats received L-NAME (50 mg/kg bw/day) in drinking water for 8 weeks.

Related Experiment Videos

  • Systolic blood pressure and heart rate were monitored weekly.
  • Cardiac hypertrophy was assessed by heart/body weight ratio and adrenergic nerve terminal density using histochemistry and Haug's point counting method.

    • Main Results:

    • L-NAME administration significantly increased systolic blood pressure.
    • Heart rate remained unchanged, but heart/body weight ratio increased markedly, indicating cardiac hypertrophy.
    • Adrenergic nerve terminal density in the left ventricle and septum decreased, while no significant changes were observed in the left atrium and right ventricle.

    Conclusions:

    • Long-term inhibition of nitric oxide synthase leads to hypertension and cardiac hypertrophy in rats.
    • Hypertension-induced cardiac hypertrophy is associated with a reduced density of adrenergic nerve terminals in the overloaded left ventricle and septum.
    • These findings suggest structural alterations in cardiac autonomic innervation in response to NO deficiency and subsequent cardiac stress.