ArticleThe Journal of clinical investigation2003
Hypertension and prolonged vasoconstrictor signaling in RGS2-deficient mice.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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Who cites it
105 citing papers in PubMed, 330 citations in OpenAlex.
- Although myeloid-cell RGS2 knockout does not affect Ang II-induced hypertension/organ damage in mice, high RGS2 in Gitelman/Bartter syndromes-human models of endogenous Ang II signaling antagonism-is associated with hypotensive/antiremodeling effects.Physiological reports · 2026Article
- The ZFP36 Family as Post-Transcriptional Regulators in Physiology and Disease.International journal of molecular sciences · 2026Review
- Conditional ablation of RGS2 in myeloid cells does not influence blood pressure and organ damage in angiotensin II-induced hypertension in mice.Physiological reports · 2026Article
- Pirfenidone Ameliorates Paraquat-Induced Epithelial-Mesenchymal Transition via miR-9-8974-5p/RGS2 Axis.Advanced biology · 2026Article
- Discovery of RGS2-FBXO44 interaction inhibitors using a cell-based NanoBit assay.Molecular pharmacology · 2025Article
- Review
- Germline deletion of Rgs2 and/or Rgs5 in male mice does not exacerbate left ventricular remodeling induced by subchronic isoproterenol infusion.Physiological reports · 2025Article
- Phosphodiesterases Mediate the Augmentation of Myogenic Constriction by Inhibitory G Protein Signaling and is Negatively Modulated by the Dual Action of RGS2 and 5.Function (Oxford, England) · 2024Article
- Common mechanisms of physiological and pathological rupture events in biology: novel insights into mammalian ovulation and beyond.Biological reviews of the Cambridge Philosophical Society · 2023Review
- Cardiometabolic Consequences of Deleting the Regulator of G protein Signaling-2 (Hypertension (Dallas, Tex. : 1979) · 2022Article
- Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide.Biology · 2022Review
- Dual loss of regulator of G protein signaling 2 and 5 exacerbates ventricular myocyte arrhythmias and disrupts the fine-tuning of GJournal of molecular and cellular cardiology · 2022Article
- Associations ofPharmaceutics · 2022Article
- Roles of Cullin-RING Ubiquitin Ligases in Cardiovascular Diseases.Biomolecules · 2022Review
- Acute and 28-days subacute toxicity studies of Gαq-RGS2 signaling inhibitor.Laboratory animal research · 2021Article
- Effect of the regulator of G-protein signaling 2 on the proliferation and invasion of oral squamous cell carcinoma cells and its molecular mechanism.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021Article
- ZHX3 promotes the progression of urothelial carcinoma of the bladder via repressing of RGS2 and is a novel substrate of TRIM21.Cancer science · 2021Article
- Pathophysiology of Hypertension: The Mosaic Theory and Beyond.Circulation research · 2021Review
- Uncovering potential differentially expressed miRNAs and targeted mRNAs in myocardial infarction based on integrating analysis.Molecular medicine reports · 2020Article
- The Role of Cullin-RING Ligases in Striated Muscle Development, Function, and Disease.International journal of molecular sciences · 2020Review
45 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signaling by hormones and neurotransmitters that activate G protein-coupled receptors (GPCRs) maintains blood pressure within the normal range despite large changes in cardiac output that can occur within seconds. This implies that blood pressure regulation requires precise kinetic control of GPCR signaling. To test this hypothesis, we analyzed mice deficient in RGS2, a GTPase-activating protein that greatly accelerates the deactivation rate of heterotrimeric G proteins in vitro. Both rgs2+/- and rgs2-/- mice exhibited a strong hypertensive phenotype, renovascular abnormalities, persistent constriction of the resistance vasculature, and prolonged response of the vasculature to vasoconstrictors in vivo. Analysis of P2Y receptor-mediated Ca2+ signaling in vascular smooth muscle cells in vitro indicated that loss of RGS2 increased agonist potency and efficacy and slowed the kinetics of signal termination. These results establish that abnormally prolonged signaling by G protein-coupled vasoconstrictor receptors can contribute to the onset of hypertension, and they suggest that genetic defects affecting the function or expression of RGS2 may be novel risk factors for development of hypertension in humans.
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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.