Effect of vagal stimulation on the overflow of norepinephrine into the coronary sinus during cardiac sympathetic nerve stimulation in the dog.
In anesthetized dogs with the chest open, supramaximal stimulation of the left cardiac sympathetic nerves at 2 and 4 Hz produced an increase of 40-50% in ventricular contractile force (CF) and of 40-65% in coronary sinus blood flow. At these frequencies of stimulation, norepinephrine (NE) overflow into the coronary sinus was 29.8 +/- 5.1 (SE) and 54.9 +/- 13.2 ng/min, respectively. Concurrent, supramaximal vagal stimulation, at a frequency of 15 Hz, had no significant effect on coronary sinus blood flow, but caused a 25% reduction in CF and a 30% decrease in NE overflow. The changes in CF and NE overflow evoked by vagal stimulation were prevented by atropine. These results are consistent with the hypothesis that there are muscarinic receptors on the postganglionic sympathetic terminals in the walls of the ventricles. Acetylcholine released during vagal stimulation combines with these receptors, causes a reduction in the liberation of NE, and thereby attenuates the positive inotropic response.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D006321:Heart / Q000294:innervation*; D006352:Heart Ventricles / Q000294:innervation; D009638:Norepinephrine / Q000378:metabolism*; D011941:Receptors, Adrenergic; D013564:Sympathetic Nervous System / Q000378:metabolism / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*
D011941:Receptors, Adrenergic; D001285:Atropine; D009638:Norepinephrine