ArticleBritish journal of pharmacology2009
Genetic disruption of G proteins, G(i2)alpha or G(o)alpha, does not abolish inotropic and chronotropic effects of stimulating muscarinic cholinoceptors in atrium.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Inotropic effects of retatrutide in isolated human atrial preparations.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Cantharidin attenuates the anti-β-adrenergic or anti-histaminergic or anti-serotoninergic effect of ANaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Inhibition of protein phosphatases attenuates ANaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Cantharidin and sodium fluoride attenuate the negative inotropic effect of the ANaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Further investigations on the influence of protein phosphatases on the signaling of muscarinic receptors in the atria of mouse hearts.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Cantharidin and sodium fluoride attenuate the negative inotropic effects of carbachol in the isolated human atrium.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Autonomic nervous system and cardiac neuro-signaling pathway modulation in cardiovascular disorders and Alzheimer's disease.Frontiers in physiology · 2023Review
- Deletion of the α subunit of the heterotrimeric Go protein impairs cerebellar cortical development in mice.Molecular brain · 2019Article
- Phenotyping of Mice with Heart Specific Overexpression of AFrontiers in pharmacology · 2018Article
- Local innervation and atrial fibrillation.Circulation · 2013Review
- Decrease in heart adrenoceptor gene expression and receptor number as compensatory tool for preserved heart function and biological rhythm in M(2) KO animals.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- Recent insights into the role of the autonomic nervous system in the creation of substrate for atrial fibrillation: implications for therapies targeting the atrial autonomic nervous system.Circulation. Arrhythmia and electrophysiology · 2012Review
- The Role of Inhibitory G Proteins and Regulators of G Protein Signaling in the in vivo Control of Heart Rate and Predisposition to Cardiac Arrhythmias.Frontiers in physiology · 2012Article
- Targeted nonviral gene-based inhibition of Gα(i/o)-mediated vagal signaling in the posterior left atrium decreases vagal-induced atrial fibrillation.Heart rhythm · 2011Article
- G protein-dependent and G protein-independent signaling pathways and their impact on cardiac function.Circulation research · 2011Review
- Augmented glucose-induced insulin release in mice lacking G(o2), but not G(o1) or G(i) proteins.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
background and purposeClassically, stimulation of muscarinic cholinoceptors exerts negative inotropic and chronotropic effects in the atrium of mammalian hearts. These effects are crucial to the vagal regulation of the heart beat. This effect is assumed to be mediated via GTP binding (G) proteins, because they can be abolished by Pertussis toxin. However, it is unknown which G proteins are involved. EXPERIMENTAL APPROACH: We studied contractility in isolated left or right atrium from genetically manipulated mice with deletion of one of two G proteins, either of the alpha subunit of G(i2) protein (G(i2)alpha) or of the alpha subunit of G(o) protein (G(o)alpha). Preparations were stimulated with carbachol alone or after pretreatment with the beta-adrenoceptor agonist isoprenaline. For comparison, the effects of carbachol on L-type Ca(2+)-channels in isolated ventricular cardiomyocytes were studied. KEY
resultsThe negative inotropic and chronotropic effects of carbachol alone or in the presence of isoprenaline were identical in atria from knockout or wild-type mice. However, the effect of carbachol on isoprenaline-activated L-type Ca(2+)-channel in isolated ventricular cardiomyocytes was greatly attenuated in both types of knockout mice studied. CONCLUSIONS AND IMPLICATIONS: These data imply that there is either redundancy of G proteins for signal transduction or that Pertussis toxin-sensitive proteins other than G(i2)alpha and G(o)alpha mediate the vagal stimulation in the atrium. Moreover, different G proteins mediate the effect of carbachol in ventricle compared with atrium.
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