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Related Experiment Videos

NO-cGMP pathway accentuates the decrease in heart rate caused by cardiac vagal nerve stimulation

C E Sears1, J K Choate, D J Paterson

  • 1University Laboratory of Physiology, Oxford OX1 3PT, United Kingdom. claire.sears@physiol.ox.ac.uk

Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 4, 1999
PubMed
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Excessive nitric oxide (NO) enhances vagal nerve stimulation

Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Regulation
  • Molecular Signaling

Background:

  • The precise role of the cardiac nitric oxide (NO) pathway in cholinergic control of heart rate (HR) remains debated.
  • Understanding this pathway is crucial for elucidating autonomic regulation of cardiac function.

Purpose of the Study:

  • To investigate how elevated nitric oxide (NO) or cyclic guanosine monophosphate (cGMP) levels influence heart rate (HR) responses to vagal nerve stimulation (VNS).
  • To determine the specific mechanisms underlying NO's modulation of cholinergic cardiac control.

Main Methods:

  • Experiments conducted in anesthetized rabbits (in vivo) and isolated guinea pig atria (in vitro).
  • Administration of NO donors (molsidomine, sodium nitroprusside) and cGMP analog (8-bromoguanosine 3',5'-cyclic monophosphate).

Related Experiment Videos

  • Vagal nerve stimulation (VNS) applied, with or without interventions, and HR responses measured. Specific antagonists (ZD-7288) and acetylcholine analogs (carbachol) used to probe mechanisms.

    • Main Results:

    • In vivo, molsidomine significantly amplified the HR decrease induced by VNS.
    • In vitro, sodium nitroprusside (SNP) produced a similar accentuation of VNS-induced bradycardia, even after blocking baseline HR shifts.
    • The effect of SNP was replicated by 8-bromoguanosine 3',5'-cyclic monophosphate but not by carbachol, suggesting a presynaptic, cGMP-dependent mechanism.

    Conclusions:

    • Excessive nitric oxide (NO) potentiates the heart rate reduction elicited by vagal nerve stimulation (VNS).
    • This potentiation appears to operate via a presynaptic mechanism involving the cyclic guanosine monophosphate (cGMP) pathway.
    • The findings clarify the intricate interplay between NO signaling and the autonomic control of heart rate.