Nerves projecting from the intrinsic cardiac ganglia of the pulmonary veins modulate sinoatrial node pacemaker function

Cardiac responses to graded treadmill exercise were compared in conscious dogs before and after excision of the sinoatrial node (SAN) and adjacent tissue along the sulcus terminalis. The chronotropic and dromotropic responses to dynamic exercise were compared with and without selective muscarinic (atropine) and/or beta-adrenergic (timolol) blockade. With the SAN intact, cardiac acceleration was prompt during onset of exercise and in proportion to work intensity. Immediately after SAN excision (1-7 days), pacemaker activity exhibited marked instability in rate and pacemaker location, with rapid shifts between atrial and junctional foci. Soon thereafter (1-2 wk), subsidiary atrial pacemakers (SAPs) assumed the primary pacemaker function. Although the SAP foci demonstrated stable heart rates and atrioventricular (AV) intervals at rest and during exercise, heart rates at rest and during steady-state exercise were reduced 34% from corresponding levels in the SAN-intact state, both with and without selective autonomic blockade. For control of dromotropic function, animals with SAP foci showed pronounced shortening in AV interval in conjunction with exercise that was further exacerbated by pretreatment with atropine. Eight weeks after excision of the primary SAN pacemakers, direct electrophysiological mapping localized the SAP foci to either the inferior right atrium along the sulcus terminalis or the dorsal cranial right atrium (in or near Bachmann's bundle). Animals with SAPs localized to the inferior right atrium had a more marked suppression in heart rate with a corresponding greater decrease in AV interval during exercise than dogs with SAP foci identified within the dorsal cranial right atrium.

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Heart Failure Differentially Modulates the Effects of Ivabradine on the Electrical Activity of the Sinoatrial Node and Pulmonary Veins

Journal of Cardiac Failure ◽

10.1016/j.cardfail.2018.09.016 ◽

2018 ◽

Vol 24 (11) ◽

pp. 763-772 ◽

Cited By ~ 4

Author(s):

Chao-Shun Chan ◽

Yao-Chang Chen ◽

Shih-Lin Chang ◽

Yung-Kuo Lin ◽

Yu-Hsun Kao ◽

...

Keyword(s):

Heart Failure ◽

Electrical Activity ◽

Sinoatrial Node ◽

Pulmonary Veins

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Differential selectivity of cardiac neurons in separate intrathoracic autonomic ganglia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.4.r939 ◽

1998 ◽

Vol 274 (4) ◽

pp. R939-R949 ◽

Cited By ~ 22

Author(s):

J. A. Armour ◽

K. Collier ◽

G. Kember ◽

J. L. Ardell

Keyword(s):

Short Term ◽

Cardiac Ganglia ◽

Intrinsic Cardiac Ganglia ◽

Cervical Ganglion ◽

The Central Nervous System ◽

Cardiac Regulation ◽

Afferent Inputs ◽

Chemical Stimuli ◽

Differential Selectivity ◽

Ganglion Neurons

Analyses of activity generated by neurons in middle cervical or stellate ganglia versus intrinsic cardiac ganglia were performed to determine how neurons in different intrathoracic ganglia, which are involved in cardiac regulation, interact. Discharges of 19% of intrathoracic extracardiac neurons and 32% of intrinsic cardiac neurons were related to cardiodynamics. Epicardial touch increased the activity generated by ∼80% of intrinsic cardiac neurons and ∼60% of extracardiac neurons. Both populations responded similarly to epicardial chemical stimuli. Activity generated by neurons in intrinsic cardiac ganglia demonstrated no consistent short-term relationships to neurons in extracardiac ganglia. Myocardial ischemia influenced extracardiac and intrinsic cardiac neurons similarly. Carotid artery baroreceptors influenced neurons in ipsilateral extracardiac ganglia. After decentralization from the central nervous system, intrinsic cardiac neurons received afferent inputs primarily from cardiac chemosensitive neurites, whereas middle cervical ganglion neurons received afferent inputs primarily from cardiac mechanosensory neurites. It is concluded that the populations of neurons in different intrathoracic ganglia can display differential reflex control of cardiac function. Their redundancy in function and noncoupled behavior minimizes cardiac dependency on a single population of intrathoracic neurons.

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Factor Xa inhibitors differently modulate electrical activities in pulmonary veins and the sinoatrial node

European Journal of Pharmacology ◽

10.1016/j.ejphar.2018.07.003 ◽

2018 ◽

Vol 833 ◽

pp. 462-471 ◽

Cited By ~ 2

Author(s):

Chien-Jung Chang ◽

Chen-Chuan Cheng ◽

Yao-Chang Chen ◽

Satoshi Higa ◽

Jen-Hung Huang ◽

...

Keyword(s):

Sinoatrial Node ◽

Pulmonary Veins ◽

Factor Xa ◽

Factor Xa Inhibitors ◽

Electrical Activities

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Heart Failure Differentially Modulates Natural (Sinoatrial Node) and Ectopic (Pulmonary Veins) Pacemakers: Mechanism and Therapeutic Implication for Atrial Fibrillation

International Journal of Molecular Sciences ◽

10.3390/ijms20133224 ◽

2019 ◽

Vol 20 (13) ◽

pp. 3224 ◽

Cited By ~ 2

Author(s):

Chao-Shun Chan ◽

Yung-Kuo Lin ◽

Yao-Chang Chen ◽

Yen-Yu Lu ◽

Shih-Ann Chen ◽

...

Keyword(s):

Heart Failure ◽

Atrial Fibrillation ◽

Electrical Activity ◽

Sinoatrial Node ◽

Sick Sinus Syndrome ◽

Pulmonary Veins ◽

Calcium Handling ◽

Adrenergic Stimulation ◽

Therapeutic Implications ◽

Cardiac Filling

Heart failure (HF) frequently coexists with atrial fibrillation (AF) and dysfunction of the sinoatrial node (SAN), the natural pacemaker. HF is associated with chronic adrenergic stimulation, neurohormonal activation, abnormal intracellular calcium handling, elevated cardiac filling pressure and atrial stretch, and fibrosis. Pulmonary veins (PVs), which are the points of onset of ectopic electrical activity, are the most crucial AF triggers. A crosstalk between the SAN and PVs determines PV arrhythmogenesis. HF has different effects on SAN and PV electrophysiological characteristics, which critically modulate the development of AF and sick sinus syndrome. This review provides updates to improve our current understanding of the effects of HF in the electrical activity of the SAN and PVs as well as therapeutic implications for AF.

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Intrinsic cardiac ganglia and acetylcholine are important in the mechanism of ischaemic preconditioning

Basic Research in Cardiology ◽

10.1007/s00395-017-0601-x ◽

2017 ◽

Vol 112 (2) ◽

Cited By ~ 29

Author(s):

J. M. J. Pickard ◽

N. Burke ◽

S. M. Davidson ◽

D. M. Yellon

Keyword(s):

Ischaemic Preconditioning ◽

Cardiac Ganglia ◽

Intrinsic Cardiac Ganglia

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Electrophysiology and pacemaker function of the developing sinoatrial node

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00750.2007 ◽

2007 ◽

Vol 293 (5) ◽

pp. H2613-H2623 ◽

Cited By ~ 19

Author(s):

Mirko Baruscotti ◽

Richard B. Robinson

Keyword(s):

Sinoatrial Node ◽

Current Knowledge ◽

Pacemaker Function ◽

Age Dependent ◽

Channel Expression ◽

Molecular Interpretation ◽

And Function ◽

Transmembrane Currents ◽

Important Evidence ◽

Nodal Tissue

The sinoatrial node performs its task as a cardiac impulse generator throughout the life of the organism, but this important function is not a constant. Rather, there are significant developmental changes in the expression and function of ion channels and other cellular elements, which lead to a postnatal slowing of heart rate and may be crucial to the reliable functioning of the node during maturation. In this review, we provide an overview of current knowledge regarding these changes, with the main focus placed on maturation of the ion channel expression profile. Studies on Na+ and pacemaker currents have shown that their contribution to automaticity is greater in the newborn than in the adult, but this age-dependent decrease is at least partially opposed by an increased contribution of L-type Ca2+ current. Whereas information regarding age-dependent changes in other transmembrane currents within the sinoatrial node are lacking, there are data on other relevant parameters. These include an increase in the nodal content of fibroblasts and in the area of nonexpression of connexin43, considered a molecular marker of nodal tissue. Although much remains to be done before a comprehensive view of the developmental biology of the node is available, important evidence in support of a molecular interpretation of developmental slowing of the intrinsic sinoatrial rate is beginning to emerge.

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