ArticleThe Journal of physiology2013
Down-regulation of CaV1.2 channels during hypertension: how fewer CaV1.2 channels allow more Ca(2+) into hypertensive arterial smooth muscle.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- The P2Y6 Receptor as a Potential Keystone in Essential Hypertension.Function (Oxford, England) · 2024Article
- α1Journal of the American Heart Association · 2024Article
- Review
- 7-Hydroxycoumarin Induces Vasorelaxation in Animals with Essential Hypertension: Focus on Potassium Channels and Intracellular CaMolecules (Basel, Switzerland) · 2022Article
- VietnameseMolecules (Basel, Switzerland) · 2022Article
- Ion channel molecular complexes in vascular smooth muscle.Frontiers in physiology · 2022Review
- Vascular smooth muscle ion channels in essential hypertension.Frontiers in physiology · 2022Review
- Chronic 3D Vascular-Immune Interface Established by Coculturing Pressurized Resistance Arteries and Immune Cells.Hypertension (Dallas, Tex. : 1979) · 2021Article
- The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.Comprehensive Physiology · 2021Article
- Calcium-Dependent Ion Channels and the Regulation of Arteriolar Myogenic Tone.Frontiers in physiology · 2021Review
- METTL3 Induces AAA Development and Progression by Modulating N6-Methyladenosine-Dependent Primary miR34a Processing.Molecular therapy. Nucleic acids · 2020Article
- Calcium Permeable Channels in Cancer Hallmarks.Frontiers in pharmacology · 2020Review
- Prenatal hypoxia plus postnatal high-fat diet exacerbated vascular dysfunction via up-regulated vascular Cav1.2 channels in offspring rats.Journal of cellular and molecular medicine · 2019Article
- Downregulation of L-Type Voltage-Gated CaJournal of the American Heart Association · 2018Article
- Inositol 1,4,5-Trisphosphate Receptors in Hypertension.Frontiers in physiology · 2018Review
- Distance constraints on activation of TRPV4 channels by AKAP150-bound PKCα in arterial myocytes.The Journal of general physiology · 2017Article
- Associations of Variants in the CACNA1A and CACNA1C Genes With Longitudinal Blood Pressure Changes and Hypertension Incidence: The GenSalt Study.American journal of hypertension · 2016Article
- Rab25 influences functional Cav1.2 channel surface expression in arterial smooth muscle cells.American journal of physiology. Cell physiology · 2016Article
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- Chronic fetal exposure to caffeine altered resistance vessel functions via RyRs-BKCa down-regulation in rat offspring.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Hypertension is a clinical syndrome characterized by increased arterial tone. Although the mechanisms are varied, the generally accepted view is that increased CaV1.2 channel function is a common feature of this pathological condition. Here, we investigated the mechanisms underlying vascular dysfunction in a mouse model of genetic hypertension. Contrary to expectation, we found that whole-cell CaV1.2 currents (ICa) were lower in hypertensive (BPH line) than normotensive (BPN line) myocytes. However, local CaV1.2 sparklet activity was higher in BPH cells, suggesting that the relatively low ICa in these cells was produced by a few hyperactive CaV1.2 channels. Furthermore, our data suggest that while the lower expression of the pore-forming α1c subunit of CaV1.2 currents underlies the lower ICa in BPH myocytes, the increased sparklet activity was due to a different composition in the auxiliary subunits of the CaV1.2 complexes. ICa currents in BPN cells were produced by channels composed of α1c/α2δ/β3 subunits, while in BPH myocytes currents were probably generated by the opening of channels formed by α1c/α2δ/β2 subunits. In addition, Ca(2+) sparks evoked large conductance, Ca(2+)-activated K(+) (BK) currents of lower magnitude in BPH than in BPN myocytes, because BK channels were less sensitive to Ca(2+). Our data are consistent with a model in which a decrease in the global number of CaV1.2 currents coexist with the existence of a subpopulation of highly active channels that dominate the resting Ca(2+) influx. The decrease in BK channel activity makes the hyperpolarizing brake ineffective and leads BPH myocytes to a more contracted resting state.
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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.