Related Experiment Video

Updated: Aug 14, 2026

Contractions of Human-iPSC-derived Cardiomyocyte Syncytia Measured with a Ca-sensitive Fluorescent Dye in Temperature-controlled 384-well Plates
07:42

Contractions of Human-iPSC-derived Cardiomyocyte Syncytia Measured with a Ca-sensitive Fluorescent Dye in Temperature-controlled 384-well Plates

Published on: October 18, 2018

Divergent action of calcium channel blockers on ATP-binding cassette protein expression

Kazuhiro Hasegawa1, Shu Wakino, Takeshi Kanda

  • 1Department of Internal Medicine, School of Medicine, Keio University, Shinanomachi, Tokyo, Japan.

Journal of Cardiovascular Pharmacology
|November 25, 2005
PubMed

Insights

Certain calcium channel blockers, like aranidipine and efonidipine, boost ATP binding cassette transporter A1 (ABCA1) protein, potentially aiding atherosclerosis treatment. This effect on ABCA1 expression differs among drug types.

Area of Science:

  • Cardiovascular Pharmacology
  • Molecular Biology
  • Atherosclerosis Research

Background:

  • Calcium channel blockers (CCBs) are clinically significant antihypertensives.
  • CCBs may play a role in preventing atherosclerosis progression.
  • ATP binding cassette transporter A1 (ABCA1) is crucial for anti-atherogenesis.

Purpose of the Study:

  • To investigate the impact of various CCBs on ABCA1 expression.
  • To elucidate the mechanisms underlying CCB-mediated ABCA1 modulation.
  • To explore potential therapeutic benefits in atherosclerosis.

Main Methods:

  • Treatment of THP-1 monocytic cells with diverse CCBs.
  • Analysis of ABCA1 protein and mRNA expression levels.
  • Assessment of signaling pathways using specific kinase inhibitors (H89, genistein, AG490) and cAMP measurement.

Main Results:

  • Aranidipine and efonidipine selectively increased ABCA1 protein, not mRNA.
  • Nifedipine, amlodipine, nicardipine, mibefradil, and nickel chloride did not affect ABCA1.
  • Protein kinase A inhibition blocked aranidipine's effect; efonidipine's mechanism remained distinct.

Conclusions:

  • Aranidipine and efonidipine differentially upregulate ABCA1 protein expression.
  • Protein kinase A mediates the effect of aranidipine on ABCA1.
  • These CCB-specific effects on ABCA1 may offer novel therapeutic strategies for hypertensive patients with atherosclerosis.

More Related Videos

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells10:46

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells

Published on: July 16, 2013

Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels07:17

Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels

Published on: December 13, 2024

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 IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...