Abstract
Cardiac vagal tone is a major determinant of health, but its origin is unknown. It is present and well developed in the decerebrate perfused working heart‐brainstem preparation (WHBP) of rat, indicating that it arises from within the brain stem. Direct recordings from the cardiac vagal branch in the WHBP (juvenile rats day 17‐25, n=10) showed spike activity that peaked in late inspiration/postinspiration, correlating with the bradycardia of respiratory sinus arrhythmia (RSA). Bilateral inhibition of neurons in the Kölliker‐Fuse nucleus (KF) of the pons by microinjections of the GABAA receptor agonist, isoguvacine (10 mM, 40‐60nl), abolished the post‐inspiratory peak but had little effect on mean cardiac vagal nerve activity. That activity assumed a tonic pattern, interrupted by brief pauses around the onset of inspiration. RSA was abolished, and heart rate rose modestly (~ 20 beats/min). Transection of the caudal pons at the level of the facial nuclei substantially reduced mean cardiac vagal activity (50‐80%) and raised heart rate substantially (~ 50 beats/min). These results indicate that cardiac vagal tone is distinct from RSA, though both depend on supramedullary connections. Drive from the KF is responsible for RSA, while the origins of most cardiac vagal tone remain to be determined.Grant Funding Source: ARC
Published Version
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