scholarly journals SCN5A and sinoatrial node pacemaker function

2007 ◽  
Vol 74 (3) ◽  
pp. 356-365 ◽  
Author(s):  
M LEI ◽  
H ZHANG ◽  
A GRACE ◽  
C HUANG
Keyword(s):  
Sinoatrial Node ◽  
Pacemaker Function

Autonomic regulation of subsidiary atrial pacemakers during exercise

1991 ◽  
Vol 70 (3) ◽  
pp. 1175-1183 ◽  
Author(s):  
J. L. Ardell ◽  
W. C. Randall ◽  
G. Pomeroy ◽  
M. Lawton ◽  
T. Kim
Keyword(s):  
Right Atrium ◽  
Sinoatrial Node ◽  
Pacemaker Activity ◽  
Work Intensity ◽  
Heart Rates ◽  
Cardiac Responses ◽  
Pacemaker Function ◽  
Before And After ◽  
Autonomic Blockade ◽  
Marked Suppression

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.

Electrophysiology and pacemaker function of the developing sinoatrial node

2007 ◽  
Vol 293 (5) ◽  
pp. H2613-H2623 ◽  
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.

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

2013 ◽  
Vol 99 (3) ◽  
pp. 566-575 ◽  
Author(s):  
Manuel Zarzoso ◽  
Kristina Rysevaite ◽  
Michelle L. Milstein ◽  
Conrado J. Calvo ◽  
Adam C. Kean ◽  
...  
Keyword(s):  
Sinoatrial Node ◽  
Pulmonary Veins ◽  
Cardiac Ganglia ◽  
Pacemaker Function ◽  
Intrinsic Cardiac Ganglia

Sophisticated Architecture is Required for the Sinoatrial Node to Perform Its Normal Pacemaker Function

2003 ◽  
Vol 14 (1) ◽  
pp. 104-106 ◽  
Author(s):  
MARK R. BOYETT ◽  
HALINA DOBRZYNSKI ◽  
MATTHEW K. LANCASTER ◽  
SANDRA A. JONES ◽  
HARUO HONJO ◽  
...  
Keyword(s):  
Sinoatrial Node ◽  
Pacemaker Function

scholarly journals CaMKII-dependent phosphorylation regulates basal cardiac pacemaker function via modulation of local Ca2+ releases

2016 ◽  
Vol 311 (3) ◽  
pp. H532-H544 ◽  
Author(s):  
Yue Li ◽  
Syevda Sirenko ◽  
Daniel R. Riordon ◽  
Dongmei Yang ◽  
Harold Spurgeon ◽  
...  
Keyword(s):  
Protein Phosphorylation ◽  
Sinoatrial Node ◽  
Ventricular Myocytes ◽  
Ryanodine Receptors ◽  
Cardiac Pacemaker ◽  
Gradual Change ◽  
Pacemaker Function ◽  
Dependent Protein ◽  
Highly Correlated ◽  
Camkii Activation

Spontaneous beating of the heart pacemaker, the sinoatrial node, is generated by sinoatrial node cells (SANC) due to gradual change of the membrane potential called diastolic depolarization (DD). Spontaneous, submembrane local Ca2+ releases (LCR) from ryanodine receptors (RyR) occur during late DD and activate an inward Na+/Ca2+exchange current to boost the DD rate and fire an action potential (AP). Here we studied the extent of basal Ca2+/calmodulin-dependent protein kinase II (CaMKII) activation and the role of basal CaMKII-dependent protein phosphorylation in generation of LCRs and regulation of normal automaticity of intact rabbit SANC. The basal level of activated (autophosphorylated) CaMKII in rabbit SANC surpassed that in ventricular myocytes (VM) by approximately twofold, and this was accompanied by high basal level of protein phosphorylation. Specifically, phosphorylation of phospholamban (PLB) at the CaMKII-dependent Thr17 site was approximately threefold greater in SANC compared with VM, and RyR phosphorylation at CaMKII-dependent Ser2815 site was ∼10-fold greater in the SA node, compared with that in ventricle. CaMKII inhibition reduced phosphorylation of PLB and RyR, decreased LCR size, increased LCR periods (time from AP-induced Ca2+ transient to subsequent LCR), and suppressed spontaneous SANC firing. Graded changes in CaMKII-dependent phosphorylation (indexed by PLB phosphorylation at the Thr17site) produced by CaMKII inhibition, β-AR stimulation or phosphodiesterase inhibition were highly correlated with changes in SR Ca2+ replenishment times and LCR periods and concomitant changes in spontaneous SANC cycle lengths ( R2 = 0.96). Thus high basal CaMKII activation modifies the phosphorylation state of Ca2+ cycling proteins PLB, RyR, L-type Ca2+ channels (and likely others), adjusting LCR period and characteristics, and ultimately regulates both normal and reserve cardiac pacemaker function.

scholarly journals IP3-mediated Ca2+ release regulates atrial Ca2+ transients and pacemaker function by stimulation of adenylyl cyclases

2021 ◽  
Vol 320 (1) ◽  
pp. H95-H107 ◽  
Author(s):  
Rebecca A. Capel ◽  
Samuel J. Bose ◽  
Thomas P. Collins ◽  
Skanda Rajasundaram ◽  
Thamali Ayagama ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Signal Transduction ◽  
Sarcoplasmic Reticulum ◽  
Future Study ◽  
Sinoatrial Node ◽  
Adenylyl Cyclases ◽  
Transduction Mechanism ◽  
Pacemaker Function ◽  
Stimulation Of ◽  
Junctional Sarcoplasmic Reticulum

This study provides evidence supporting the proposal that IP3 signaling in cardiac atria and sinoatrial node involves stimulation of Ca2+-activated adenylyl cyclases (AC1 and AC8) by IP3-evoked Ca2+ release from junctional sarcoplasmic reticulum. AC8 and IP3 receptors are shown to be located close together, while AC1 is nearby. Greater understanding of these novel aspects of the IP3 signal transduction mechanism is important for future study in atrial physiology and pathophysiology, particularly atrial fibrillation.

scholarly journals CaMKII-Dependent Phosphorylation Modulates Ca2+ Cycling in Sinoatrial Node Cells to Regulate Cardiac Pacemaker Function

2013 ◽  
Vol 104 (2) ◽  
pp. 361a-362a
Author(s):  
Tatiana M. Vinogradova ◽  
Syevda Sirenko ◽  
Yue Li ◽  
Dongmei Yang ◽  
Harold Spurgeon ◽  
...  
Keyword(s):  
Sinoatrial Node ◽  
Cardiac Pacemaker ◽  
Pacemaker Function ◽  
Sinoatrial Node Cells

scholarly journals Tbx3 controls the sinoatrial node gene program and imposes pacemaker function on the atria

2007 ◽  
Vol 21 (9) ◽  
pp. 1098-1112 ◽  
Author(s):  
W. M.H. Hoogaars ◽  
A. Engel ◽  
J. F. Brons ◽  
A. O. Verkerk ◽  
F. J. de Lange ◽  
...  
Keyword(s):  
Sinoatrial Node ◽  
Pacemaker Function

scholarly journals Genetic Complexity of Sinoatrial Node Dysfunction

2021 ◽  
Vol 12 ◽  
Author(s):  
Michael J. Wallace ◽  
Mona El Refaey ◽  
Pietro Mesirca ◽  
Thomas J. Hund ◽  
Matteo E. Mangoni ◽  
...  
Keyword(s):  
Sinoatrial Node ◽  
Sinus Bradycardia ◽  
Pacemaker Implantation ◽  
Heart Rhythm ◽  
The Elderly ◽  
Pacemaker Function ◽  
Cardiac Pacemaking ◽  
Mechanistic Basis ◽  
Cardiac Automaticity ◽  
Sinoatrial Node Dysfunction

The pacemaker cells of the cardiac sinoatrial node (SAN) are essential for normal cardiac automaticity. Dysfunction in cardiac pacemaking results in human sinoatrial node dysfunction (SND). SND more generally occurs in the elderly population and is associated with impaired pacemaker function causing abnormal heart rhythm. Individuals with SND have a variety of symptoms including sinus bradycardia, sinus arrest, SAN block, bradycardia/tachycardia syndrome, and syncope. Importantly, individuals with SND report chronotropic incompetence in response to stress and/or exercise. SND may be genetic or secondary to systemic or cardiovascular conditions. Current management of patients with SND is limited to the relief of arrhythmia symptoms and pacemaker implantation if indicated. Lack of effective therapeutic measures that target the underlying causes of SND renders management of these patients challenging due to its progressive nature and has highlighted a critical need to improve our understanding of its underlying mechanistic basis of SND. This review focuses on current information on the genetics underlying SND, followed by future implications of this knowledge in the management of individuals with SND.

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