Potassium rectifier currents differ in myocytes of endocardial and epicardial origin.

Furukawa, Tetsushi; Kimura, Shin-ichi; Furukawa, N; Bassett, Arthur L.; Myerburg, Robert J.

doi:10.1161/01.res.70.1.91

Cited by 98 publications

(49 citation statements)

References 34 publications

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“…However, in guinea pig, I Ks and I Kr are smaller in subendocardial myocytes than in mid-and subepicardial myocytes. 39 Furthermore, inward rectifying current (I K1 ) is smaller in cat subepicardium 50 but not in subepicardium of guinea pig 51 and dog. 52 The transmural gradient in action potential duration found in isolated myocytes is present in isolated perfused ventricular wedge preparations of the dog heart as well, especially at long cycle lengths.…”

Section: Transmural Heterogeneity In Action Potential Durationmentioning

confidence: 96%

Developmental Basis for Electrophysiological Heterogeneity in the Ventricular and Outflow Tract Myocardium As a Substrate for Life-Threatening Ventricular Arrhythmias

Boukens

Christoffels

Coronel

et al. 2009

Circulation Research

132

102

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Abstract-Reentry is the main mechanism of life-threatening ventricular arrhythmias, including ventricular fibrillation and tachycardia. Its occurrence depends on the simultaneous presence of an arrhythmogenic substrate (a preexisting condition) and a "trigger," and is favored by electrophysiological heterogeneities. In the adult heart, electrophysiological heterogeneities of the ventricle exist along the apicobasal, left-right, and transmural axes. Also, conduction is preferentially slowed in the right ventricular outflow tract, especially during pharmacological sodium channel blockade. We propose that the origin of electrophysiological heterogeneities of the adult heart lies in early heart development. The heart is formed from several progenitor regions: the first heart field predominantly forms the left ventricle, whereas the second heart field forms the right ventricle and outflow tract. Furthermore, the embryonic outflow tract consists of slowly conducting tissue until it is incorporated into the ventricles and develops rapidly conducting properties. The subepicardial myocytes and subendocardial myocytes run distinctive gene programs from their formation onwards. This review discusses the hypothesis that electrophysiological heterogeneities in the adult heart result from persisting patterns in gene expression and function along the craniocaudal and epicardial-endocardial axes of the developing heart. Understanding the developmental origins of electrophysiological heterogeneity contributing to ventricular arrhythmias may give rise to new therapies.

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Section: Transmural Heterogeneity In Action Potential Durationmentioning

confidence: 96%

Developmental Basis for Electrophysiological Heterogeneity in the Ventricular and Outflow Tract Myocardium As a Substrate for Life-Threatening Ventricular Arrhythmias

Boukens

Christoffels

Coronel

et al. 2009

Circulation Research

132

102

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“…On repolarization each current trace is followed by a slowly decaying current tail. This current has been identified as the delayed rectifying current (IK) (Follmer & Colatsky, 1990;Furukawa et al, 1992). Berberine decreased the current activated during the depolarizing pulse and the subsequent tail current.…”

Section: Single Cell Isolationmentioning

confidence: 99%

“…In cat ventricular myocytes using the 'envelope of tails test', the delayed rectifier current has been found to be composed of a single component (Furukawa et al, 1992). In addition, Follmer & Colatsky (1990) have found that IK in cat ventricular myocytes is completely blocked by E-403 1, suggesting that only IKs is present in this preparation.…”

Section: Introductionmentioning

confidence: 96%

Increase in action potential duration and inhibition of the delayed rectifier outward current I_K by berberine in cat ventricular myocytes

Sánchez-Chapula

1996

British J Pharmacology

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1In the present work, the effects of the antiarrhythmic drug, berberine, on action potential and ionic currents of cat ventricular myocytes were studied. 2 Berberine prolonged action potential duration in cat ventricular myocytes without altering other variables of the action potential. 3 The drug at concentrations of 0.3-30 gM blocked only the delayed rectifier (IK) current with an IC50 = 4.1 gM. Berberine produced a tonic block and a phasic block that was increased with the duration of the depolarizing pulse. The blocking effect on IK was use-dependent, but not frequency-dependent. 4 In cardiac preparations two delayed rectifier currents have been found: a rapid ('Kr) current and a slow (IKs) current. In the present work it has been found that berberine at the concentrations used, selectively blocked IKr 5 At concentrations higher than 10 gM it also decreased the transient outward (Itol) current. The drug did not have effects on the inward rectifier (IKI) or the high threshold calcium current ('CaL).6 These results show that berberine is a specific potassium channel blocker. The increase in action potential duration induced by berberine can be explained mainly by its blocking effects on IK-

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“…[12][13][14][15][16] In particular, we have shown previously 17 that systematic heterogeneities of APD restitution between cells across the epicardial surface govern, in a coupling-interval-dependent fashion, premature stimulus-induced modulation of spatial gradients of repolarization. Because spatial gradients of repolarization are closely associated with reentrant arrhythmogenesis, 3,18 modulation of such gradients may play an important role in the mechanisms of cardiac arrhythmias.…”

mentioning

confidence: 92%

Modulated Dispersion Explains Changes in Arrhythmia Vulnerability During Premature Stimulation of the Heart

et al. 1998

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Background-Previously, we have shown that a premature stimulus can significantly modulate spatial gradients of ventricular repolarization (ie, modulated dispersion), which result from heterogeneous electrophysiological properties between cells. The role modulated dispersion may play in determining electrical instability in the heart is unknown. Methods and Results-To determine if premature stimulus-induced changes in repolarization are a mechanism that governs susceptibility to cardiac arrhythmias, optical action potentials were recorded simultaneously from 128 ventricular sites (1 cm 2 ) in 8 Langendorff-perfused guinea pig hearts. After baseline pacing (S 1 ), a single premature stimulus (S 2 ) was introduced over a range of S 1 S 2 coupling intervals. Arrhythmia vulnerability after each premature stimulus was determined by measurement of a modified ventricular fibrillation threshold (VFT) during the T wave of each S 2 beat (ie, S 2 -VFT). As the S 1 S 2 interval was shortened to an intermediate value, spatial gradients of repolarization and vulnerability to fibrillation decreased by 51Ϯ9% (meanϮSEM) and 73Ϯ45%, respectively, compared with baseline levels. As the S 1 S 2 interval was further shortened, repolarization gradients increased above baseline levels by 54Ϯ30%, which was paralleled by a corresponding increase (37Ϯ8%) in vulnerability.Conclusions-These data demonstrate that modulation of repolarization gradients by a single premature stimulus significantly influences vulnerability to ventricular fibrillation. This may represent a novel mechanism for the formation of arrhythmogenic substrates during premature stimulation of the heart. (Circulation. 1998;98:2774-2780.)

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Potassium rectifier currents differ in myocytes of endocardial and epicardial origin.

Cited by 98 publications

References 34 publications

Developmental Basis for Electrophysiological Heterogeneity in the Ventricular and Outflow Tract Myocardium As a Substrate for Life-Threatening Ventricular Arrhythmias

Developmental Basis for Electrophysiological Heterogeneity in the Ventricular and Outflow Tract Myocardium As a Substrate for Life-Threatening Ventricular Arrhythmias

Increase in action potential duration and inhibition of the delayed rectifier outward current I_K by berberine in cat ventricular myocytes

Modulated Dispersion Explains Changes in Arrhythmia Vulnerability During Premature Stimulation of the Heart

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Potassium rectifier currents differ in myocytes of endocardial and epicardial origin.

Cited by 98 publications

References 34 publications

Developmental Basis for Electrophysiological Heterogeneity in the Ventricular and Outflow Tract Myocardium As a Substrate for Life-Threatening Ventricular Arrhythmias

Developmental Basis for Electrophysiological Heterogeneity in the Ventricular and Outflow Tract Myocardium As a Substrate for Life-Threatening Ventricular Arrhythmias

Increase in action potential duration and inhibition of the delayed rectifier outward current IK by berberine in cat ventricular myocytes

Modulated Dispersion Explains Changes in Arrhythmia Vulnerability During Premature Stimulation of the Heart

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Increase in action potential duration and inhibition of the delayed rectifier outward current I_K by berberine in cat ventricular myocytes