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

Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
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...
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists01:23

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

Serotonin, a crucial neurotransmitter synthesized by enterochromaffin cells, plays a cardinal role in regulating gastrointestinal (GI) motility. With over 90% of the body's total serotonin in the GI tract, its influence on digestive processes is profound. Serotonin is swiftly released upon various stimuli, such as food boluses or certain drugs, triggering intrinsic sensory neurons in the myenteric plexus and extrinsic vagal and spinal sensory neurons. This leads to the activation of the...

You might also read

Related Articles

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

Sort by
Same author

On indirect negative inotropic effects of muscarine in the isolated human atrium.

Naunyn-Schmiedeberg's archives of pharmacology·2026
Same author

Mechanisms of systolic heart failure in PP2CxPP5 double transgenic mice.

Naunyn-Schmiedeberg's archives of pharmacology·2026
Same author

Contractile effects of dulaglutide in the human atrium.

Naunyn-Schmiedeberg's archives of pharmacology·2026
Same author

Protein phosphatase 2A impairs cardiac uptake of glucose in the mammalian heart.

Naunyn-Schmiedeberg's archives of pharmacology·2026
Same author

Acute Contractile Effects of Glucagon-like-Peptide-1 Receptor Agonists in the Human Heart.

Pharmaceutics·2026
Same author

Positive inotropic and chronotropic effects of amisulpride via stimulation of 5-HT<sub>4</sub> serotonin receptors in the isolated atrium from mouse and humans.

Naunyn-Schmiedeberg's archives of pharmacology·2026

Related Experiment Video

Updated: Jul 8, 2026

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b
10:20

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b

Published on: November 11, 2016

Imipramine Can Block Human Cardiac H 1 -Histamine Receptors.

Thanh Hoai Pham1, Britt Hofmann2, Jonas M A Schlicht1

  • 1Institute for Pharmacology and Toxicology, Medical Faculty, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.

Journal of Cardiovascular Pharmacology
|July 7, 2026
PubMed
Summary

Imipramine, an antidepressant, was found to antagonize histamine H1 receptor effects on heart contraction. This finding in mice and human heart tissue may explain cardiac side effects of imipramine.

Keywords:
hearthistamineinotropy

More Related Videos

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
08:11

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

Published on: November 11, 2022

Stepwise Dosing Protocol for Increased Throughput in Label-Free Impedance-Based GPCR Assays
06:13

Stepwise Dosing Protocol for Increased Throughput in Label-Free Impedance-Based GPCR Assays

Published on: February 21, 2020

Related Experiment Videos

Last Updated: Jul 8, 2026

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b
10:20

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b

Published on: November 11, 2016

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
08:11

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

Published on: November 11, 2022

Stepwise Dosing Protocol for Increased Throughput in Label-Free Impedance-Based GPCR Assays
06:13

Stepwise Dosing Protocol for Increased Throughput in Label-Free Impedance-Based GPCR Assays

Published on: February 21, 2020

Area of Science:

  • Pharmacology
  • Cardiology
  • Neuroscience

Background:

  • Imipramine is a widely used antidepressant affecting noradrenaline and serotonin.
  • Imipramine exhibits high-affinity binding to histamine H1 receptors.
  • Histamine H1 receptor stimulation increases cardiac contractility.

Purpose of the Study:

  • To investigate if imipramine antagonizes histamine H1 receptor-mediated positive inotropic effects in the heart.
  • To determine the effect of imipramine on H1-histamine receptor stimulation in genetically modified mice and human atrial tissue.

Main Methods:

  • Utilized genetically modified mice overexpressing the human H1-histamine receptor (H1-TG).
  • Studied human right atrial muscle preparations from cardiac surgery patients.
  • Administered imipramine and observed its effect on H1-histamine receptor agonist-induced contractions.

Main Results:

  • Imipramine reduced force of contraction in H1-TG mouse atria starting at 100 nM.
  • Imipramine antagonized H1-histamine receptor stimulation effects in human atrial preparations starting at 300 nM.
  • These effects were consistent with imipramine's interaction with H1-histamine receptors.

Conclusions:

  • Imipramine antagonizes H1-histamine receptor-mediated positive inotropic effects in mammalian atria.
  • Imipramine's action on the human atrium suggests a mechanism for observed cardiac side effects.
  • This study links antidepressant action to cardiac histamine receptor modulation.