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 248: H33-H39, 1985;
0363-6135/85 $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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wetzel, G. T.
Right arrow Articles by Brown, J. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wetzel, G. T.
Right arrow Articles by Brown, J. H.

AJP - Heart and Circulatory Physiology, Vol 248, Issue 1 33-H39, Copyright © 1985 by American Physiological Society

ARTICLES

Presynaptic modulation of acetylcholine release from cardiac parasympathetic neurons

G. T. Wetzel and J. H. Brown

Acetylcholine can be released from parasympathetic nerve endings in rat atria by 57 mM K+ depolarization or by electrical field stimulation. We have studied the presynaptic modulation of [3H]acetylcholine release from superfused rat atria prelabeled with [3H]choline. Exogenous acetylcholine and the specific muscarinic agonist oxotremorine inhibit the stimulation-induced overflow of [3H]acetylcholine into the superfusion medium. The half-maximal inhibitory concentration (IC50) of oxotremorine is 0.3 microM. The cholinesterase inhibitor neostigmine also decreases K+-stimulated [3H]acetylcholine overflow, whereas the muscarinic antagonist atropine enhances the overflow of [3H]acetylcholine. These data suggest that acetylcholine release in atria is modulated through negative feedback by the endogenous transmitter. The sympathetic adrenergic neurotransmitter norepinephrine and the neurohormone epinephrine also inhibit the overflow of [3H]acetylcholine by approximately 60%. The IC50 values for the inhibitory effects of these catecholamines are 6.3 and 2.2 microM, respectively. The inhibitory effect of norepinephrine is blocked by the alpha-adrenergic receptor antagonist yohimbine but not by the beta-adrenergic receptor antagonist propranolol. We suggest that presynaptic muscarinic and alpha-adrenergic receptors participate in the physiological and pharmacological control of cardiac parasympathetic activity.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. Arora, J. S. Ulphani, R. Villuendas, J. Ng, L. Harvey, S. Thordson, F. Inderyas, Y. Lu, D. Gordon, P. Denes, et al.
Neural substrate for atrial fibrillation: implications for targeted parasympathetic blockade in the posterior left atrium
Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H134 - H144.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
T. Miyamoto, T. Kawada, Y. Yanagiya, M. Inagaki, H. Takaki, M. Sugimachi, and K. Sunagawa
Cardiac sympathetic nerve stimulation does not attenuate dynamic vagal control of heart rate via {alpha}-adrenergic mechanism
Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H860 - H865.
[Abstract] [Full Text] [PDF]


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