Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2008;118:863-871
doi: 10.1161/CIRCULATIONAHA.107.760405
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Olshansky, B.
Right arrow Articles by Colucci, W. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Olshansky, B.
Right arrow Articles by Colucci, W. S.
Related Collections
Right arrow Cardio-renal physiology/pathophysiology
Right arrow Congestive
Right arrow Other Treatment

(Circulation. 2008;118:863-871.)
© 2008 American Heart Association, Inc.


Contemporary Reviews in Cardiovascular Medicine

Parasympathetic Nervous System and Heart Failure

Pathophysiology and Potential Implications for Therapy

Brian Olshansky, MD; Hani N. Sabbah, PhD; Paul J. Hauptman, MD; Wilson S. Colucci, MD

From the Division of Cardiology, University of Iowa Hospitals, Iowa City (B.O.); Cardiovascular Medicine, Henry Ford Health System, Detroit, Mich (H.N.S.); Department of Medicine, Saint Louis University School of Medicine, St Louis, Mo (P.J.H.); and Department of Medicine, Boston University School of Medicine, Boston, Mass (W.S.C.).

Correspondence to Brian Olshansky, MD, University of Iowa Hospitals, 200 Hawkins Dr 4426a JCP, Iowa City, IA 52242. E-mail brian-olshansky@uiowa.edu


Key Words: heart failure • nervous system, autonomic • parasympathetic nervous system • pathophysiology


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
Abundant evidence links sympathetic nervous system activation to outcomes of patients with heart failure (HF).1 In contrast, parasympathetic activation has complex cardiovascular effects that are only beginning to be recognized. In particular, the pathophysiological roles of normal and disordered parasympathetic innervation in patients with HF are not understood as comprehensively.2–5

In the present article, we review cardiovascular responses to parasympathetic activation, address the modulating factors that can affect parasympathetic function, discuss the role of the vagus nerve in ventricular dysfunction, and consider how activation of the parasympathetic nervous system may have important therapeutic implications for patients with congestive HF.


*    Structure of the Parasympathetic Limb of the Autonomic Nervous System
 
The parasympathetic nervous system originates from medial medullary sites (nucleus ambiguous, nucleus tractus solitarius, and dorsal motor nucleus) and is modulated by the hypothalamus. Vagal efferents extend from the medulla to postganglionic nerves that innervate the atria via ganglia located in cardiac fat pads with neurotransmission that is modulated via nicotinic receptors. Postganglionic parasympathetic and sympathetic cholinergic nerves then affect cardiac muscarinic receptors (the Figure).6–8


Figure Removed (Available Only in the Full Text)
View larger version (67K):



 
Figure. Parasympathetic and sympathetic innervation of the heart: anatomy. Efferent fiber (vagus) comprises A-beta, A-delta, and unmyelinated C fibers. Reproduced from Martini FH. Fundamentals of Anatomy and Physiology. 8th ed. 2006. Chapter 20, by permission of Pearson Education, Inc Prentice Hall, copyright © 2006.

Vagus nerve afferent activation, originating peripherally, can modulate efferent sympathetic and parasympathetic function centrally and at the level of the baroreceptor.

Efferent vagus nerve activation can have tonic and basal effects that inhibit sympathetic activation and release of norepinephrine at . . . [Full Text of this Article]




This article has been cited by other articles:


Home page
CirculationHome page
M. Ahmadi-Kashani, D. J. Kessler, J. Day, T. J. Bunch, K. Q. Stolen, S. Brown, S. Sbaity, B. Olshansky, and on behalf of the INTRINSIC RV Study Investigators
Heart Rate Predicts Outcomes in an Implantable Cardioverter-Defibrillator Population
Circulation, November 24, 2009; 120(21): 2040 - 2045.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
F. Triposkiadis, G. Karayannis, G. Giamouzis, J. Skoularigis, G. Louridas, and J. Butler
The sympathetic nervous system in heart failure physiology, pathophysiology, and clinical implications.
J. Am. Coll. Cardiol., November 3, 2009; 54(19): 1747 - 1762.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
J. C. Hardwick, C. N. Baran, E. M. Southerland, and J. L. Ardell
Remodeling of the guinea pig intrinsic cardiac plexus with chronic pressure overload
Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2009; 297(3): R859 - R866.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
B. Olshansky, R. Gopinathannair, and R. M. Sullivan
DAVID II did not slay Goliath.
J. Am. Coll. Cardiol., March 10, 2009; 53(10): 881 - 883.
[Full Text] [PDF]