AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 241: H684-H690, 1981;
0363-6135/81 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Loeb, J. M.
Right arrow Articles by Moran, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Loeb, J. M.
Right arrow Articles by Moran, J. M.

AJP - Heart and Circulatory Physiology, Vol 241, Issue 5 684-H690, Copyright © 1981 by American Physiological Society


ARTICLES

Sensitivity differences of SA and AV node to vagal stimulation: attenuation of vagal effects at SA node

J. M. Loeb, D. P. Dalton and J. M. Moran

The present study sought to characterize vagally induced desensitization at the sinoatrial (SA) node of the intact dog and to determine whether these findings could be extended to atrioventricular (AV) Nodal conduction. Autonomically decentralized anesthetized dogs were instrumented to record electrocardiograms, arterial pressure, and electrograms from the SA node, right atrium, right ventricle, and His bundle. During right- or left-vagal stimulation for 60 s, cycle length (CL) increased initially, followed by a gradual recovery toward control during stimulation; atrio-His (AH) interval remained prolonged throughout the stimulation. Atrial drive increased AH interval during stimulation, but AH prolongation was maintained throughout the stimulation period. To rule out acetylcholine (ACh) depletion, ACh was administered before and during vagal stimulation. Although control CL and AH interval were lengthened by ACh, no significant CL increases occurred when ACh was given during stimulation, but the AH interval became longer. Propranolol increased control CL and AH interval but did not alter the relationship between vagal stimulation and CL or AH interval. Thus the negative chronotropic effect of ACh at the SA node is diminished upon prolonged vagal stimulation, whereas the negative dromotropic effect upon AV nodal conduction remains unaltered. These results suggest differences in muscarinic receptor behavior at the SA and AV nodes.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online