December 8, 2011Journal of Molecular and Cellular CardiologyOpen Access

The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: Implications for neural control of cardiac excitability

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Population

Isolated guinea pig atrial preparation with dual autonomic innervation and stellate ganglion tissue

Design

Preclinical

Authors

NHNeil HerringElectrophysiology JCJames CranleyWellcome/MRC Cambridge Stem Cell Institute MLMichael N. LokaleUniversity of Oxford

Discussion

Member takes

Implication

May explain vagal impairment in HF; leaves open GalR1 antagonism as a therapeutic target pending human studies.

Structured PICO

Population

Isolated guinea pig atrial preparation with dual autonomic innervation and stellate ganglion tissue

Intervention

Prolonged right stellate ganglion stimulation (10 Hz, 2 min, in the presence of 10 μM metoprolol) and exogenous galanin (50-500 nM)

Outcome

Magnitude of vagal bradycardia and acetylcholine releasesurrogate

The sympathetic co-transmitter galanin contributes to impaired vagal bradycardia by reducing acetylcholine release, providing a potential mechanism for the autonomic imbalance seen in heart failure.

Cite This Study

Herring et al. (2011) studied this question.

synapsesocial.com/papers/6a70b30cf44fa9f079de634e https://doi.org/10.1016/j.yjmcc.2011.11.016

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The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: Implications for neural control of cardiac excitability

Discussion

Member takes

Implication

Structured PICO

Cite This Study

The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: Implications for neural control of cardiac excitability

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider