Related Experiment Video

Updated: Aug 18, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Indapamide blocks the rapid component of the delayed rectifier current in atrial tumor cells (AT-1 cells)

S M Kabir1, M L Bhattacharyya, T R Robinson

  • 1Department of Anatomy and Physiology, Meharry Medical College, Nashville, TN 37208, USA.

International Journal of Cardiology
|April 5, 2000
PubMed

Insights

Indapamide, a known blocker of the slow component of the delayed rectifier potassium current (I(ks)), also inhibits the rapid component (I(kr)) in atrial tumor myocytes. This diuretic agent demonstrates a dose-dependent blockade of these crucial cardiac currents.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Pharmacology

Background:

  • Atrial tumor myocytes (AT-1 cells) from transgenic mice express cardiac K(+) channel mRNAs and exhibit electrophysiological properties.
  • The primary potassium current in these cells is the rapid component of the delayed rectifier (I(kr)).

Purpose of the Study:

  • To investigate the effects of indapamide, a selective blocker of the slow component of the delayed rectifier (I(ks)), on cardiac K(+) currents.
  • To determine if indapamide also blocks the rapid component of the delayed rectifier (I(kr)) in a dose-dependent manner.

Main Methods:

  • Utilized the one-electrode voltage clamp technique to record K(+) currents.
  • Employed AT-1 cells derived from transgenic mice to study electrophysiological phenotypes.
  • Administered varying concentrations of indapamide to assess its blocking effects.

Main Results:

  • Indapamide significantly reduced steady-state currents (I(1s)) and tail currents (I(tail)) in a dose-dependent manner.
  • At 750 microM, indapamide decreased I(1s) from 1070.4+/-202.2 pA to 254.5+/-62.3 pA and I(tail) from 416.3+/-112.9 pA to 42.2+/-37.7 pA.
  • The observed blockade by indapamide showed partial reversibility at higher concentrations (≥750 microM).

Conclusions:

  • Indapamide acts as a blocker for both the slow (I(ks)) and rapid (I(kr)) components of the delayed rectifier potassium current in atrial tumor myocytes.
  • The diuretic agent indapamide exhibits a dose-dependent inhibitory effect on cardiac K(+) currents, specifically targeting I(kr).
  • These findings highlight indapamide's broader impact on cardiac electrophysiology beyond its known action on I(ks).

More Related Videos

Isolation of Atrial Myocytes from Adult Mice08:34

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

Optimization of Transesophageal Atrial Pacing to Assess Atrial Fibrillation Susceptibility in Mice08:05

Optimization of Transesophageal Atrial Pacing to Assess Atrial Fibrillation Susceptibility in Mice

Published on: June 29, 2022

Related Concept Videos

Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...
Cardiac Action Potential01:30

Cardiac Action Potential

Cardiac action potentials are essential for proper heart function, enabling the rhythmic contractions needed for adequate blood circulation. Nodal cells and Purkinje fibers, specialized for electrical conduction, generate these action potentials.
The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
Ionic Basis of Cardiac Action Potentials
Dysrhythmias IV: Characteristics of Bradyarrhythmias01:18

Dysrhythmias IV: Characteristics of Bradyarrhythmias

Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...