ArticleJournal of the American Society of Hypertension : JASH
Vascular Smooth Muscle Cell Signaling Mechanisms for Contraction to Angiotensin II and Endothelin-1.
Article in Journal of the American Society of Hypertension : JASH. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
97 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- Guidelines for the isolation and characterization of murine vascular smooth muscle cells. A report from the International Society of Cardiovascular Translational Research.Journal of cardiovascular translational research · 2015Guideline
- Efficacy and safety of skin-adhesive low-level light therapy for overactive bladder: a Phase III study.International urogynecology journal · 2022Trial
- Review
- Neuro-Mechanical Regulation of Vascular Smooth Muscle Cell Behaviour Under Ageing-Associated Substrate Stiffness.Current issues in molecular biology · 2026Article
- Developmental and Structural Alterations at the Ductus-Aortic Isthmus Interface in Infantile Coarctation of the Aorta: A Biological Basis for Persistent Vascular Disease Beyond Anatomical Repair.Journal of clinical medicine · 2026Article
- Melatonin alleviates diabetic-induced vascular dysfunction by modulating endothelin-1 receptors (ETA and ETB) reactivity in rat aortic rings.Acta diabetologica · 2026Article
- KPharmaceuticals (Basel, Switzerland) · 2026Review
- Smooth Muscle LRRC8A Knockout Preserves Vascular Function in Ang II Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026Article
- The multifactorial role of HDAC9 at the maternal-fetal interface in the pathogenesis of preeclampsia.Clinical science (London, England : 1979) · 2025Review
- BaPharmacology research & perspectives · 2025Article
- Oxidized LDL enhances Gq signaling and aldosterone production by angiotensin II via the AT1-LOX-1 receptor complex in adrenal cells.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Epigenetic alteration of smooth muscle cells regulates endothelin-dependent blood pressure and hypertensive arterial remodeling.The Journal of clinical investigation · 2025Article
- Pericyte and Endothelial Cell Responses within Murine Cerebral Capillaries After Blood Flow Cessation.bioRxiv : the preprint server for biology · 2025Article
- Trifolin inhibits the calcium-driven contraction pathway in vascular smooth muscle.Frontiers in pharmacology · 2025Article
- Imperatorin's Effect on Myocardial Infarction Based on Network Pharmacology and Molecular Docking.Cardiovascular therapeutics · 2025Article
- The role and mechanism of vascular wall cell ion channels in vascular fibrosis remodeling.Channels (Austin, Tex.) · 2024Review
- α1Journal of the American Heart Association · 2024Article
- Article
- Phospholipase C-β3 is dispensable for vascular constriction but indispensable for vascular hyperplasia.Experimental & molecular medicine · 2024Article
- The Enigma of Norbormide, aCells · 2024Review
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Vasoactive peptides, such as endothelin-1 and angiotensin II are recognized by specific receptor proteins located in the cell membrane of target cells. Following receptor recognition, the specificity of the cellular response is achieved by G-protein coupling of ligand binding to the regulation of intracellular effectors. These intracellular effectors will be the subject of this brief review on contractile activity initiated by endothelin-1 and angiotensin II.Activation of receptors by endothelin-1 and angiotensin II in smooth muscle cells results in phopholipase C (PLC) activation leading to the generation of the second messengers insitol trisphosphate (IP(3)) and diacylglycerol (DAG). IP(3) stimulates intracellular Ca(2+) release from the sarcoplasmic reticulum and DAG causes protein kinase C (PKC) activation. Additionally, different Ca(2+) entry channels, such as voltage-operated (VOC), receptor-operated (ROC), and store-operated (SOC) Ca(2+) channels, as well as Ca(2+)-permeable nonselective cation channels (NSCC), are involved in the elevation of intracellular Ca(2+) concentration. The elevation in intracellular Ca(2+) is transient and initiates contractile activity by a Ca(2+)-calmodulin interaction, stimulating myosin light chain (MLC) phosphorylation. When the Ca(2+) concentration begins to decline, Ca(2+)-sensitization of the contractile proteins is signaled by the RhoA/Rho-kinase pathway to inhibit the dephosphorylation of MLC phosphatase (MLCP) thereby maintaining force generation. Removal of Ca(2+) from the cytosol and stimulation of MLCP initiates the process of smooth muscle relaxation. In pathological conditions such as hypertension, alterations in these cellular signaling components can lead to an over stimulated state causing maintained vasoconstriction and blood pressure elevation.
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Registered trials
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.