ArticleBritish journal of pharmacology2015
GPCR dimerization in brainstem nuclei contributes to the development of hypertension.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Atomic, structural and molecular insights into GPCR ligand binding and signalling.Nature reviews. Molecular cell biology · 2026Review
- Correlation of G protein-coupled receptor and tumor microenvironment with gastric cancer outcomes and therapies.Chinese medical journal · 2026Article
- G protein-coupled receptors: a gateway to targeting oncogenic EVs?Extracellular vesicles and circulating nucleic acids · 2024Review
- Multi-omics identification of GPCR gene features in lung adenocarcinoma based on multiple machine learning combinations.Journal of Cancer · 2024Article
- Detecting and measuring of GPCR signaling - comparison of human induced pluripotent stem cells and immortal cell lines.Frontiers in endocrinology · 2023Review
- Drug-Targeted Genomes: Mutability of Ion Channels and GPCRs.Biomedicines · 2022Article
- Review
- μ-Opioid Receptor-Mediated AT1R-TLR4 Crosstalk Promotes Microglial Activation to Modulate Blood Pressure Control in the Central Nervous System.Antioxidants (Basel, Switzerland) · 2021Article
- Mu Opioid Receptor Heterodimers Emerge as Novel Therapeutic Targets: Recent Progress and Future Perspective.Frontiers in pharmacology · 2020Review
- Heteromerization Modulates mu Opioid Receptor Functional PropertiesFrontiers in pharmacology · 2018Review
- Preeclampsia and the brain: neural control of cardiovascular changes during pregnancy and neurological outcomes of preeclampsia.Clinical science (London, England : 1979) · 2016Review
- Dual allosteric modulation of opioid antinociceptive potency by α2A-adrenoceptors.Neuropharmacology · 2015Article
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Authors and funding
10 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeμ-Opioid receptors, pro-opiomelanocortin and pro-enkephalin are highly expressed in the nucleus tractus solitarii (NTS) and μ receptor agonists given to the NTS dose-dependently increased BP. However, the molecular mechanisms of this process remain unclear. In vitro, μ receptors heterodimerize with α2A -adrenoceptors. We hypothesized that α2A -adrenoceptor agonists would lose their depressor effects when their receptors heterodimerize in the NTS with μ receptors. EXPERIMENTAL APPROACH: We microinjected μ-opioid agonists and antagonists into the NTS of rats and measured changes in BP. Formation of μ receptor/α2A -adrenoceptor heterodimers was assessed with immunofluorescence and co-immunoprecipitation methods, along with proximity ligation assays. KEY
resultsImmunofluorescence staining revealed colocalization of α2A -adrenoceptors and μ receptors in NTS neurons. Co-immunoprecipitation revealed interactions between α2A -adrenoceptors and μ receptors. In situ proximity ligation assays confirmed the presence of μ receptor/α2A -adrenoceptor heterodimers in the NTS. Higher levels of endogenous endomorphin-1 and μ receptor/α2A -adrenoceptor heterodimers were found in the NTS of hypertensive rats, than in normotensive rats. Microinjection of the μ receptor agonist [D-Ala(2) , MePhe(4) , Gly(5) -ol]-enkephalin (DAMGO), but not that of the α2A -adrenoceptor agonist guanfacine, into the NTS of normotensive rats increased μ receptor/α2A -adrenoceptor heterodimer formation and BP elevation. The NO-dependent BP-lowering effect of α2A -adrenoceptor agonists was blunted following increased formation of μ receptor/α2A -adrenoceptor heterodimers in the NTS of hypertensive rats and DAMGO-treated normotensive rats. CONCLUSIONS AND IMPLICATIONS: Increases in endogenous μ receptor agonists in the NTS induced μ receptor/α2A -adrenoceptor heterodimer formation and reduced the NO-dependent depressor effect of α2A -adrenoceptor agonists. This process could contribute to the pathogenesis of hypertension.
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