Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...
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 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 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...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Heterogeneity after harmonisation: A retrospective cohort study of bleeding and stroke risk after the introduction of direct oral anticoagulants in four Western European countries.

Pharmacoepidemiology and drug safety·2023
Same author

Comparison of calibrated dilute thrombin time and aPTT tests with LC-MS/MS for the therapeutic monitoring of patients treated with dabigatran etexilate.

Thrombosis and haemostasis·2013
Same author

Autologous low density lipoprotein enhances platelet aggregation in whole blood, as measured by in vitro filtragometry.

Platelets·2010
Same author

Decreased fibrin network permeability and impaired fibrinolysis in the acute and convalescent phase of ischemic stroke.

Thrombosis research·2010
Same author

Poor performance with a platelet counting technique to monitor clopidogrel inhibitory effects in the point-of-care setting.

Thrombosis research·2009
Same author

Influence of statin treatment on platelet inhibition by clopidogrel - a randomized comparison of rosuvastatin, atorvastatin and simvastatin co-treatment.

Journal of internal medicine·2009

Related Experiment Video

Updated: Jul 12, 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

Calcium antagonist treatment, sympathetic activity and platelet function

P Hjemdahl1, N H Wallén

  • 1Department of Clinical Pharmacology, Karolinska Hospital, Stockholm, Sweden.

European Heart Journal
|January 1, 1997
PubMed
Summary

Calcium antagonists have varied effects on neuro-hormonal activity and platelet function, often indirectly. Further research is needed to fully understand these drug class impacts.

More Related Videos

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
10:28

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Published on: March 15, 2022

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
07:13

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Related Experiment Videos

Last Updated: Jul 12, 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

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
10:28

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Published on: March 15, 2022

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
07:13

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Area of Science:

  • Pharmacology
  • Cardiovascular Medicine

Background:

  • Calcium antagonists are a diverse drug class with indirect effects on neuro-hormonal activity and platelet function.
  • Their impact is not solely due to L-type calcium channel inhibition, necessitating a broader understanding.

Purpose of the Study:

  • To review the heterogeneous effects of calcium antagonists on neuro-hormonal activity and platelet function.
  • To highlight the need for more detailed in vivo studies to accurately assess these effects.

Main Methods:

  • Review of existing literature on calcium antagonist effects.
  • Analysis of studies concerning sympathetic activity and platelet function.

Main Results:

  • Vascularly selective dihydropyridines can increase heart rate and sympathetic activity, which may persist long-term.
  • Heart-rate reducing agents show variable effects on sympathetic activity; verapamil and diltiazem differ.
  • In vitro antiplatelet effects do not always translate to clinical relevance, and results are inconsistent.

Conclusions:

  • Calcium antagonist effects on neuro-hormonal and platelet function are complex and indirect.
  • Generalizing findings from one calcium antagonist to another is not advisable due to drug class heterogeneity.
  • More rigorous in vivo studies are required to elucidate the precise mechanisms and clinical relevance of these effects.