Action Potential Remodeling in the Human Right Atrium with Chronic Lone Atrial Fibrillation

Conventional microelectrode recordings combined with enzymatic cell dispersion methods and a single microelectrode voltage-clamp technique were used to record transmembrane action potentials and ionic currents in isolated single myocytes and in excised segments of human right atrium. Recordings of the outward current(s), which is responsible for the resting potential and early repolarization of the action potential in human right atrium, consistently showed that this tissue has 1) a relatively small inwardly rectifying background potassium current (IK1) which generates the resting potential in mammalian ventricular tissue and Purkinje fibers, and 2) a large time- and voltage-dependent, but Ca2(+)-independent, transient outward current. A somewhat similar K+ current was originally described in neurons and recently has also been identified in a variety of mammalian cardiac tissues. As expected from previous work, this transient outward current in human atrium is blocked by 4-aminopyridine (4-AP; 0.5 mM) and exhibits time- and voltage-dependent inactivation and reactivation. Measurements of action potential shape changes and phasic tension as a function of stimulus frequency, or after 4-AP application, show that in human atrium this current can produce pronounced changes in both the early repolarization of the action potential and force generation.

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A 5-HT4-like receptor in human right atrium

Naunyn-Schmiedeberg s Archives of Pharmacology ◽

10.1007/bf00167212 ◽

1991 ◽

Vol 344 (2) ◽

pp. 150-159 ◽

Cited By ~ 78

Author(s):

Alberto J. Kaumann ◽

Louise Sanders ◽

Anthony M. Brown ◽

Kenneth J. Murray ◽

Morris J. Brown

Keyword(s):

Right Atrium ◽

Human Right ◽

Human Right Atrium

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Urotensin II receptor expression in human right atrium and aorta: effects of ischaemic heart disease

British Journal of Anaesthesia ◽

10.1093/bja/aep011 ◽

2009 ◽

Vol 102 (4) ◽

pp. 477-484 ◽

Cited By ~ 5

Author(s):

A.D. Leonard ◽

J.P. Thompson ◽

E.L. Hutchinson ◽

S.P. Young ◽

J. McDonald ◽

...

Keyword(s):

Heart Disease ◽

Ischaemic Heart Disease ◽

Right Atrium ◽

Receptor Expression ◽

Urotensin Ii ◽

Human Right ◽

Human Right Atrium

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The repolarization-excitability relationship in the human right atrium is unaffected by cycle length, recording site and prior arrhythmias

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(00)01189-x ◽

2001 ◽

Vol 37 (3) ◽

pp. 920-925 ◽

Cited By ~ 30

Author(s):

Frank Bode ◽

Michael Kilborn ◽

Pamela Karasik ◽

Michael R Franz

Keyword(s):

Right Atrium ◽

Cycle Length ◽

Recording Site ◽

Human Right ◽

Human Right Atrium

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From cellular automata model of vagal control of the human right atrium to heart beats patterns

Physica D Nonlinear Phenomena ◽

10.1016/j.physd.2020.132771 ◽

2021 ◽

Vol 415 ◽

pp. 132771

Author(s):

Danuta Makowiec ◽

Wiesław Miklaszewski ◽

Joanna Wdowczyk ◽

Anna T. Lawniczak

Keyword(s):

Cellular Automata ◽

Right Atrium ◽

Human Right ◽

Cellular Automata Model ◽

Vagal Control ◽

Human Right Atrium

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Acetylcholine release by a stimulus train lowers atrial fibrillation threshold

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.4.h863 ◽

1987 ◽

Vol 253 (4) ◽

pp. H863-H868 ◽

Cited By ~ 2

Author(s):

D. E. Euler ◽

P. J. Scanlon

Keyword(s):

Atrial Fibrillation ◽

Action Potential ◽

Right Atrium ◽

Single Pulse ◽

Monophasic Action Potential ◽

Adrenergic Blockade ◽

The Right ◽

Alpha Chloralose ◽

Electrical Stimuli ◽

Local Release

This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.

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Prostacyclins have no direct inotropic effect on isolated atrial strips from the normal and pressure-overloaded human right heart

Pulmonary Circulation ◽

10.1177/2045893217691532 ◽

2017 ◽

Vol 7 (2) ◽

pp. 339-347 ◽

Cited By ~ 5

Author(s):

Sarah Holmboe ◽

Asger Andersen ◽

Rebekka V. Jensen ◽

Hans Henrik Kimose ◽

Lars B. Ilkjær ◽

...

Keyword(s):

Right Atrium ◽

Quantitative Polymerase Chain Reaction ◽

Organ Bath ◽

Inotropic Response ◽

Force Of Contraction ◽

Human Right ◽

Prostanoid Receptors ◽

Right Heart ◽

Inotropic Effects ◽

Human Right Atrium

Prostacyclins are vasodilatory agents used in the treatment of pulmonary arterial hypertension. The direct effects of prostacyclins on right heart function are still not clarified. The aim of this study was to investigate the possible direct inotropic properties of clinical available prostacyclin mimetics in the normal and the pressure-overloaded human right atrium. Trabeculae from the right atrium were collected during surgery from chronic thromboembolic pulmonary hypertension (CTEPH) patients with pressure-overloaded right hearts, undergoing pulmonary thromboendarterectomy (n = 10) and from patients with normal right hearts operated by valve replacement or coronary bypass surgery (n = 9). The trabeculae were placed in an organ bath, continuously paced at 1 Hz. They were subjected to increasing concentrations of iloprost, treprostinil, epoprostenol, or MRE-269, followed by isoprenaline to elicit a reference inotropic response. The force of contraction was measured continuously. The expression of prostanoid receptors was explored through quantitative polymerase chain reaction (qPCR). Iloprost, treprostinil, epoprostenol, or MRE-269 did not alter force of contraction in any of the trabeculae. Isoprenaline showed a direct inotropic response in both trabeculae from the pressure-overloaded right atrium and from the normal right atrium. Control experiments on ventricular trabeculae from the pig failed to show an inotropic response to the prostacyclin mimetics. qPCR demonstrated varying expression of the different prostanoid receptors in the human atrium. In conclusion, prostacyclin mimetics did not increase the force of contraction of human atrial trabeculae from the normal or the pressure-overloaded right heart. These data suggest that prostacyclin mimetics have no direct inotropic effects in the human right atrium.

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