September 1, 2001The Journal of PhysiologyOpen Access

Nitric oxide‐cGMP pathway facilitates acetylcholine release and bradycardia during vagal nerve stimulation in the guinea‐pig in vitro

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Population

Isolated guinea-pig atrial-right vagal nerve preparations

Comparison

Sodium nitroprusside 10 microM, with or without… vs Control conditions

Design

Preclinical

Authors

NHNeil HerringElectrophysiology DPDavid J. PatersonUnited States Nuclear Regulatory Commission

Discussion

Member takes

Implication

Preclinical findings support NO facilitation of vagal bradycardia; hypothesis-generating for human autonomic regulation.

Structured PICO

Population

Isolated guinea-pig atrial-right vagal nerve preparations

Intervention

Sodium nitroprusside (SNP) 10 microM, with or without various enzyme inhibitors and calcium channel blockers (ODQ, milrinone, KT5823, H-89, KT5720, omega-conotoxin GVIA)

Comparator

Control conditions (absence of SNP or specific inhibitors)

Outcome

Heart rate response to vagal nerve stimulation and release of [3H]acetylcholinesurrogate

Nitric oxide acts presynaptically to facilitate vagal neurotransmission and bradycardia via a cGMP-PDE 3-dependent pathway leading to cAMP-PKA-dependent phosphorylation of N-type calcium channels.

Cite This Study

Herring et al. (2001) studied this question.

synapsesocial.com/papers/6a704a61a528af2d65c370a7 https://doi.org/10.1111/j.1469-7793.2001.00507.x

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Nitric oxide‐cGMP pathway facilitates acetylcholine release and bradycardia during vagal nerve stimulation in the guinea‐pig in vitro

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Nitric oxide‐cGMP pathway facilitates acetylcholine release and bradycardia during vagal nerve stimulation in the guinea‐pig in vitro

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider