ArticleCardiovascular diabetology2023
Evidence for a lack of inotropic and chronotropic effects of glucagon and glucagon receptors in the human heart.
Article in Cardiovascular diabetology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- An experimental medicine protocol for exploring the haemodynamic effects of dual agonism at the glucagon-like peptide-1 and glucagon receptor in healthy subjects.British journal of clinical pharmacology · 2026Trial
- Exenatide and glucagon co-infusion increases myocardial glucose uptake and improves markers of diastolic dysfunction in adults with type 2 diabetes.Scientific reports · 2025Trial
- Cardiac neurons expressing a glucagon-like receptor mediate cardiac arrhythmia induced by high-fat diet ineLife · 2026Article
- Metabolomic Biomarkers for Non-Invasive Diagnosis of Coronary Artery Disease and Obstructive Sleep Apnea Co-Occurrence.Nature and science of sleep · 2026Article
- Inotropic effects of retatrutide in isolated human atrial preparations.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Glucagon Can Increase Force of Contraction via Glucagon Receptors in the Isolated Human Atrium.International journal of molecular sciences · 2025Article
- Physiological Appetite Regulation and Bariatric Surgery.Journal of clinical medicine · 2024Review
- Glucagon and Its Receptors in the Mammalian Heart.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlucagon is thought to increase heart rate and contractility by stimulating glucagon receptors and increasing 3',5'-cyclic adenosine monophosphate (cAMP) production in the myocardium. This has been confirmed in animal studies but not in the human heart. The cardiostimulatory effects of glucagon have been correlated with the degree of cardiac dysfunction, as well as with the enzymatic activity of phosphodiesterase (PDE), which hydrolyses cAMP. In this study, the presence of glucagon receptors in the human heart and the inotropic and chronotropic effects of glucagon in samples of failing and nonfailing (NF) human hearts were investigated.
methodsConcentration‒response curves for glucagon in the absence and presence of the PDE inhibitor IBMX were performed on samples obtained from the right (RA) and left atria (LA), the right (RV) and left ventricles (LV), and the sinoatrial nodes (SNs) of failing and NF human hearts. The expression of glucagon receptors was also investigated. Furthermore, the inotropic and chronotropic effects of glucagon were examined in rat hearts.
resultsIn tissues obtained from failing and NF human hearts, glucagon did not exert inotropic or chronotropic effects in the absence or presence of IBMX. IBMX (30 µM) induced a marked increase in contractility in NF hearts (RA: 83 ± 28% (n = 5), LA: 80 ± 20% (n = 5), RV: 75 ± 12% (n = 5), and LV: 40 ± 8% (n = 5), weaker inotropic responses in the ventricular myocardium of failing hearts (RV: 25 ± 10% (n = 5) and LV: 10 ± 5% (n = 5) and no inotropic responses in the atrial myocardium of failing hearts. IBMX (30 µM) increased the SN rate in failing and NF human hearts (27.4 ± 3.0 beats min
conclusionsOur results conflict with the view that glucagon induces inotropic and chronotropic effects and that glucagon receptors are expressed in the human heart.
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