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

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining. Bicarbonate,...
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
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...

You might also read

Related Articles

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

Sort by
Same author

Dyskalemia in people at increased risk for heart failure: findings from the heart 'OMics' in AGEing (HOMAGE) trial.

ESC heart failure·2022
Same author

Periostin Augments Vascular Smooth Muscle Cell Calcification via β-Catenin Signaling.

Biomolecules·2022
Same author

Nitric oxide metabolites: associations with cardiovascular biomarkers and clinical parameters in patients with HFpEF.

ESC heart failure·2022
Same author

Light at the end of the tunnel? : Diagnostic and therapeutic strategies for heart failure with preserved ejection fraction.

Herz·2022
Same author

Vericiguat and NT-proBNP in patients with heart failure with reduced ejection fraction: analyses from the VICTORIA trial.

ESC heart failure·2022
Same author

Effects of BNP and Sacubitrilat/Valsartan on Atrial Functional Reserve and Arrhythmogenesis in Human Myocardium.

Frontiers in cardiovascular medicine·2022

Related Experiment Video

Updated: Jul 12, 2026

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine
10:05

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

Published on: July 7, 2016

Negative inotropy of the gastric proton pump inhibitor pantoprazole in myocardium from humans and rabbits: evaluation

Wolfgang Schillinger1, Nils Teucher, Samuel Sossalla

  • 1Herzzentrum, Kardiologie und Pneumologie, Georg-August Universitaet Goettingen, Robert-Koch Strasse 40, 37099 Goettingen, Germany. schiwolf@med.uni-goettingen.de

Circulation
|June 20, 2007
PubMed
Summary

Pantoprazole, a common acid reflux medication, was found to decrease cardiac contractility in heart cells. Further in vivo studies are needed to assess these effects in living organisms.

More Related Videos

Isolation of Human Ventricular Cardiomyocytes from Vibratome-Cut Myocardial Slices
11:19

Isolation of Human Ventricular Cardiomyocytes from Vibratome-Cut Myocardial Slices

Published on: May 10, 2020

Translational Rabbit Model of Chronic Cardiac Pacing
06:14

Translational Rabbit Model of Chronic Cardiac Pacing

Published on: January 6, 2023

Related Experiment Videos

Last Updated: Jul 12, 2026

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine
10:05

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

Published on: July 7, 2016

Isolation of Human Ventricular Cardiomyocytes from Vibratome-Cut Myocardial Slices
11:19

Isolation of Human Ventricular Cardiomyocytes from Vibratome-Cut Myocardial Slices

Published on: May 10, 2020

Translational Rabbit Model of Chronic Cardiac Pacing
06:14

Translational Rabbit Model of Chronic Cardiac Pacing

Published on: January 6, 2023

Area of Science:

  • Cardiology
  • Pharmacology
  • Molecular Biology

Background:

  • Proton pump inhibitors (PPIs) are widely prescribed for gastrointestinal acid-related disorders.
  • The direct impact of PPIs on cardiac contractility remains largely uninvestigated.

Purpose of the Study:

  • To investigate the direct effects of pantoprazole on cardiac contractility.
  • To elucidate the underlying mechanisms of pantoprazole's action on cardiac function.

Main Methods:

  • Isolated human and rabbit cardiac tissues (ventricular and atrial trabeculae) and myocytes were used.
  • Contractile force, intracellular calcium (Ca2+) transients, L-type Ca2+ current (I(Ca,L)), and sarcoplasmic reticulum Ca2+ ATPase activity were measured.
  • Real-time polymerase chain reaction was employed to detect gastric H+/K+-adenosine triphosphatase expression in cardiac tissue.

Main Results:

  • Pantoprazole induced a dose-dependent reduction in contractile force in human and rabbit cardiac preparations.
  • Measurements revealed depressed Ca2+ signaling, including reduced Ca2+ transient amplitude and impaired sarcoplasmic reticulum Ca2+ uptake.
  • Pantoprazole diminished the Ca2+-activated force of cardiac myofilaments and reduced I(Ca,L) amplitude.

Conclusions:

  • Pantoprazole exerts a direct negative inotropic effect on cardiac contractility in vitro.
  • The observed cardiac depression is attributed to impaired Ca2+ signaling and myofilament responsiveness.
  • Clinical evaluation of pantoprazole's cardiovascular effects in vivo is warranted due to its widespread use.