ArticleBritish journal of pharmacology2003
Cardiac-specific overexpression of human beta2 adrenoceptors in mice exposes coupling to both Gs and Gi proteins.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Roles of Catecholamines and Inflammation in Endothelial Dysfunction: a Study Using Takotsubo Syndrome Patient-specific hiPSC-ECs.Stem cell reviews and reports · 2026Article
- Takotsubo syndrome: Unraveling the mystery behind its triggers (Review).International journal of molecular medicine · 2025Review
- Review
- Functional optimization of light-activatable Opto-GPCRs: Illuminating the importance of the proximal C-terminus in G-protein specificity.Frontiers in cell and developmental biology · 2023Article
- Molecular Mechanisms of Takotsubo Syndrome.International journal of molecular sciences · 2022Review
- βArrestins in cardiac G protein-coupled receptor signaling and function: partners in crime or "good cop, bad cop"?International journal of molecular sciences · 2013Review
- GRK2 blockade with βARKct is essential for cardiac β2-adrenergic receptor signaling towards increased contractility.Cell communication and signaling : CCS · 2013Article
- Noradrenaline stimulates cell proliferation by suppressing potassium channels via G(i/o) -protein-coupled α(1B) -adrenoceptors in human osteoblasts.British journal of pharmacology · 2013Article
- High levels of circulating epinephrine trigger apical cardiodepression in a β2-adrenergic receptor/Gi-dependent manner: a new model of Takotsubo cardiomyopathy.Circulation · 2012Article
- Ser/ Thr residues at α3/β5 loop of Gαs are important in morphine-induced adenylyl cyclase sensitization but not mitogen-activated protein kinase phosphorylation.The FEBS journal · 2012Article
- The Effects of β (2) -Adrenoreceptor Activation on the Contractility, Ca-Signals and Nitric Oxide Production in the Mouse Atria.Acta naturae · 2011Article
- Expression of a G protein-coupled receptor (GPCR) leads to attenuation of signaling by other GPCRs: experimental evidence for a spontaneous GPCR constitutive inactive form.The Journal of biological chemistry · 2010Article
- Beta1-adrenergic receptors stimulate cardiac contractility and CaMKII activation in vivo and enhance cardiac dysfunction following myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2009Article
- Activation of Gi induces mechanical hyperalgesia poststress or inflammation.Neuroscience · 2009Article
- Metabolic responses to BRL37344 and clenbuterol in soleus muscle and C2C12 cells via different atypical pharmacologies and beta2-adrenoceptor mechanisms.British journal of pharmacology · 2008Article
- Switching of G-protein usage by the calcium-sensing receptor reverses its effect on parathyroid hormone-related protein secretion in normal versus malignant breast cells.The Journal of biological chemistry · 2008Article
- Stress induces a switch of intracellular signaling in sensory neurons in a model of generalized pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Beta(2)-Adrenergic activation increases glycogen synthesis in L6 skeletal muscle cells through a signalling pathway independent of cyclic AMP.Diabetologia · 2007Article
- Multiple signalling pathways involved in beta2-adrenoceptor-mediated glucose uptake in rat skeletal muscle cells.British journal of pharmacology · 2006Article
- The ups and downs of Gs- to Gi-protein switching.British journal of pharmacology · 2003Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Left atrial strips from transgenic (TG4) mice with cardiac-specific overexpression ( approximately 200-fold) of the beta(2) adrenoceptor (beta(2)AR) were isolated, and their isometric force of contraction (F(c)) in response to electrical stimulation was measured. 2. The betaAR agonist isoprenaline elicited negative inotropic responses in all left atrial strips; in 6/11 preparations, it also had a small positive inotropic effect. This 'up-phase' was observed from 0.1 to 10 nM, with the 'down-phase' occurring at higher concentrations. Both phases were mediated by beta(2)AR, as shown by their sensitivity to the beta(2)AR antagonist ICI-118,551 (100 nM; pA(2) 8.60+/-0.07, 8.45+/-0.19, for 'up-phase' and 'down-phase,' respectively), but not the beta(1)AR antagonist CGP-20712A (100 nM). Conversely, nontransgenic littermate preparations responded to isoprenaline treatment solely by an increase in F(c), which was beta(1)AR-mediated. 3. Pretreatment of left atrial strips with either 10 nM isoprenaline or 1 mM 8-bromo-cAMP significantly attenuated the TG4 'up-phase', while having no effect on either the TG4 'down-phase' or the littermate controls' responses. B. pertussis toxin treatment of the animals prevented isoprenaline's negative inotropic effects in TG4 preparations, but had no effect in littermate controls. 4. The findings imply that the responses of TG4 left atrium to isoprenaline are because of beta(2)AR coupling to G(s) and G(i) proteins, consistent with the model of Daaka et al., in which protein kinase A phosphorylation of the beta(2)AR causes a switch from G(s) to G(i) protein coupling.
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