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Related Experiment Videos

Heart rate dynamics in iNOS knockout mice.

Ali R Mani1, Richard Ollosson, Yasaman Mani

  • 1The UCL Institute of Hepatology, Department of Medicine, Royal Free and University College Medical School, UCL, London, Rowland Hill Street London NW3 2PF, UK. a.mani@medsch.ucl.ac.uk

Life Sciences
|June 23, 2006
PubMed
Summary

Mice lacking the inducible nitric oxide synthase (iNOS) gene exhibit increased cardiac sympathetic activity, as shown by heart rate variability analysis. This study also found that lipopolysaccharide-induced reductions in heart rate variability are independent of iNOS.

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Area of Science:

  • Cardiovascular physiology
  • Autonomic nervous system regulation
  • Nitric oxide signaling

Background:

  • Nitric oxide (NO) plays a dual role in regulating sympathetic neurons, with inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) mediating inhibitory and excitatory effects, respectively.
  • Understanding the specific roles of iNOS in cardiovascular autonomic control is crucial, particularly in conditions like endotoxemia.

Purpose of the Study:

  • To investigate the impact of iNOS gene disruption on cardiovascular autonomic activity using heart rate variability (HRV) spectral analysis in mice.
  • To elucidate the role of iNOS in the alterations of HRV observed during endotoxemia.

Main Methods:

  • Recording electrocardiograms in anesthetized wild-type and iNOS knockout mice.
  • Digitizing R-R intervals for spectral analysis of HRV and sample entropy analysis to assess cardiac rhythm regularity.

Related Experiment Videos

  • Administering lipopolysaccharide (LPS) to induce endotoxemia and evaluating its effects on HRV.

    • Main Results:

    • iNOS knockout mice displayed a higher basal heart rate and significantly increased low-frequency power in HRV spectra, indicating enhanced cardiac sympathetic activity.
    • LPS administration elevated heart rate in both wild-type and iNOS knockout mice but depressed HRV and sample entropy in both groups.
    • Experiments with isolated beating atria demonstrated that HRV changes under basal or post-LPS conditions were abolished in vitro, confirming the involvement of the autonomic nervous system.

    Conclusions:

    • Disruption of the iNOS gene results in elevated low-frequency HRV power, consistent with increased cardiac sympathetic activity.
    • The decrease in HRV induced by LPS is independent of the iNOS system.
    • These findings highlight the specific role of iNOS in modulating basal sympathetic tone and its dissociation from LPS-induced HRV depression.