Vagal action on atrioventricular conduction and its inhibition by sympathetic stimulation and neuropeptide Y in anaesthetised dogs.
The observed change in atrioventricular conduction time (PR interval) in response to vagal stimulation is the result of two opposing effects; PR interval increases in response to the direct action of the vagus on atrioventricular nodal cells (direct effect), and the accompanying slowing of heart rate acts to decrease PR interval (indirect effect). The relationships between these opposing effects were studied in anaesthetised dogs. This study has shown that the increase in PR interval in response to vagal stimulation is well correlated with vagal stimulation frequency and can be regarded as linear. This is so for unpaced and paced hearts. We have also shown there is an increase in the sensitivity of the relationship between increase in PR interval and vagal stimulation frequency during pacing. This increase in sensitivity is attributable to the elimination of the indirect effect of the slowing of heart rate. During atrial pacing, the relationship between pulse interval and PR interval resembles a hyperbola. At low-pulse intervals (i.e. fast heart rates) the PR interval increases. This is in agreement with previous qualitative findings and is related to the functional refractory period of the atrioventricular cells. The action of sympathetic stimulation and injection of neuropeptide Y has not been studied previously. The vagally induced increase in atrioventricular conduction time is attenuated for many minutes following stimulation of the cardiac sympathetic nerve at 16 Hz for 2 min or by intravenous injection of neuropeptide Y (25-50 micrograms/kg). Stimulation of the right cardiac sympathetic nerve evokes a significantly stronger inhibition of the vagally induced prolongation of pulse interval than stimulation of the left sympathetic nerve. On the other hand, stimulation of the left or right sympathetic nerves cause similar inhibition of vagal action on atrioventricular conduction time.
Pirola
F T
FT
School of Physiology and Pharmacology, University of New South Wales, Kensington, Sydney, Australia.
Potter
E K
EK
D000818:Animals; D001283:Atrioventricular Node / Q000502:physiology*; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D008297:Male; D009433:Neural Inhibition; D009478:Neuropeptide Y / Q000494:pharmacology*; D011674:Pulse / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000502:physiology*; D013997:Time Factors; D014630:Vagus Nerve / Q000502:physiology*
D009478:Neuropeptide Y