ArticleBritish journal of pharmacology2008
5-HT4-elicited positive inotropic response is mediated by cAMP and regulated by PDE3 in failing rat and human cardiac ventricles.
Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Prokinetic drugs that stimulate 5-HTNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Tegaserod Stimulates 5-HTInternational journal of molecular sciences · 2024Article
- Zacopride stimulates 5-HTNaunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Cardiac Roles of Serotonin (5-HT) and 5-HT-Receptors in Health and Disease.International journal of molecular sciences · 2023Review
- Phosphodiesterases and Compartmentation of cAMP and cGMP Signaling in Regulation of Cardiac Contractility in Normal and Failing Hearts.International journal of molecular sciences · 2022Review
- Phosphodiesterases 2, 3 and 4 can decrease cardiac effects of HNaunyn-Schmiedeberg's archives of pharmacology · 2021Article
- International Union of Basic and Clinical Pharmacology. CX. Classification of Receptors for 5-hydroxytryptamine; Pharmacology and Function.Pharmacological reviews · 2021Review
- Which phosphodiesterase can decrease cardiac effects of 5-HTNaunyn-Schmiedeberg's archives of pharmacology · 2019Article
- cAMP Catalyzing Phosphodiesterases Control Cholinergic Muscular Activity But Their Inhibition Does Not Enhance 5-HTFrontiers in pharmacology · 2018Article
- The effects of serotonin on the electrophysiological properties of atrioventricular node during an experimental atrial fibrillation.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Inhibition of phosphodiesterase-3 by levosimendan is sufficient to account for its inotropic effect in failing human heart.British journal of pharmacology · 2014Article
- Differential regulation of C-type natriuretic peptide-induced cGMP and functional responses by PDE2 and PDE3 in failing myocardium.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- Cardiac PDEs and crosstalk between cAMP and cGMP signalling pathways in the regulation of contractility.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Influence of phosphodiesterases and cGMP on cAMP generation and on phosphorylation of phospholamban and troponin I by 5-HT4 receptor activation in porcine left atrium.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Spatial control of the βAR system in heart failure: the transverse tubule and beyond.Cardiovascular research · 2013Review
- The cardiac ventricular 5-HT4 receptor is functional in late foetal development and is reactivated in heart failure.PloS one · 2012Article
- Agents increasing cyclic GMP amplify 5-HT4-elicited positive inotropic response in failing rat cardiac ventricle.Naunyn-Schmiedeberg's archives of pharmacology · 2011Article
- Conserved expression and functions of PDE4 in rodent and human heart.Basic research in cardiology · 2011Article
- Differential regulation of β2 -adrenoceptor-mediated inotropic and lusitropic response by PDE3 and PDE4 in failing and non-failing rat cardiac ventricle.British journal of pharmacology · 2011Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe left ventricle in failing hearts becomes sensitive to 5-HT parallelled by appearance of functional G(s)-coupled 5-HT(4) receptors. Here, we have explored the regulatory functions of phosphodiesterases in the 5-HT(4) receptor-mediated functional effects in ventricular muscle from failing rat and human heart. EXPERIMENTAL APPROACH: Extensive myocardial infarctions were induced by coronary artery ligation in Wistar rats. Contractility was measured in left ventricular papillary muscles of rat, 6 weeks after surgery and in left ventricular trabeculae from explanted human hearts. cAMP was quantified by RIA. KEY
resultsIn papillary muscles from postinfarction rat hearts, 5-HT(4) stimulation exerted positive inotropic and lusitropic effects and increased cAMP. The inotropic effect was increased by non-selective PDE inhibition (IBMX, 10 microM) and selective inhibition of PDE3 (cilostamide, 1 microM), but not of PDE2 (EHNA, 10 microM) or PDE4 (rolipram, 10 microM). Combined PDE3 and PDE4 inhibition enhanced inotropic responses beyond the effect of PDE3 inhibition alone, increased the sensitivity to 5-HT, and also revealed an inotropic response in control (sham-operated) rat ventricle. Lusitropic effects were increased only during combined PDE inhibition. In failing human ventricle, the 5-HT(4) receptor-mediated positive inotropic response was regulated by PDEs in a manner similar to that in postinfarction rat hearts. CONCLUSIONS AND IMPLICATIONS: 5-HT(4) receptor-mediated positive inotropic responses in failing rat ventricle were cAMP-dependent. PDE3 was the main PDE regulating this response and involvement of PDE4 was disclosed by concomitant inhibition of PDE3 in both postinfarction rat and failing human hearts. 5-HT, PDE3 and PDE4 may have pathophysiological functions in heart failure.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.