ArticlePflugers Archiv : European journal of physiology2014
TMEM16A knockdown abrogates two different Ca(2+)-activated Cl (-) currents and contractility of smooth muscle in rat mesenteric small arteries.
Article in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Loss of Vascular TMEM16A Impairs Cerebral Autoregulation and Exacerbates Ischemia-reperfusion Injury.Translational stroke research · 2026Article
- CaActa physiologica (Oxford, England) · 2026Review
- TMEM16A channel signalling microdomains in the regulation of vascular function.The Journal of physiology · 2026Review
- Acidosis enhances contribution of CaCurrent research in physiology · 2025Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Myography of isolated blood vessels: Considerations for experimental design and combination with supplementary techniques.Frontiers in physiology · 2023Review
- Chloride Ions, Vascular Function and Hypertension.Biomedicines · 2022Review
- A small molecule inhibitor of the chloride channel TMEM16A blocks vascular smooth muscle contraction and lowers blood pressure in spontaneously hypertensive rats.Kidney international · 2021Article
- Calcium-Activated Chloride Channels in Myometrial and Vascular Smooth Muscle.Frontiers in physiology · 2021Review
- Trophic sympathetic influence weakens pro-contractile role of ClScientific reports · 2020Article
- A paradoxical increase of force development in saphenous and tail arteries from heterozygous ANO1 knockout mice.Physiological reports · 2020Article
- Calcium-Activated Chloride Channel ANO1/TMEM16A: Regulation of Expression and Signaling.Frontiers in physiology · 2020Review
- Ion channels and the regulation of myogenic tone in peripheral arterioles.Current topics in membranes · 2020Review
- Smooth muscle CaJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- TMEM16A is implicated in the regulation of coronary flow and is altered in hypertension.British journal of pharmacology · 2019Article
- Ano1 mediates pressure-sensitive contraction frequency changes in mouse lymphatic collecting vessels.The Journal of general physiology · 2019Article
- Ultrasensitive Photonic Microsystem Enabling Sub-micrometric Monitoring of Arterial Oscillations for Advanced Cardiovascular Studies.Frontiers in physiology · 2019Article
- Targeted sequencing identifies a missense variant in the BEST3 gene associated with antihypertensive response to hydrochlorothiazide.Pharmacogenetics and genomics · 2018Article
- Transmembrane member 16A participates in hydrogen peroxide-induced apoptosis by facilitating mitochondria-dependent pathway in vascular smooth muscle cells.British journal of pharmacology · 2018Article
- Murine breast cancer feed arteries are thin-walled with reduced αBreast cancer research : BCR · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The presence of Ca(2+)-activated Cl(-) channels (CaCCs) in vascular smooth muscle cells (SMCs) is well established. Their molecular identity is, however, elusive. Two distinct Ca(2+)-activated Cl(-) currents (I Cl(Ca)) were previously characterized in SMCs. We have shown that the cGMP-dependent I Cl(Ca) depends on bestrophin expression, while the "classical" I Cl(Ca) is not. Downregulation of bestrophins did not affect arterial contraction but inhibited the rhythmic contractions, vasomotion. In this study, we have used in vivo siRNA transfection of rat mesenteric small arteries to investigate the role of a putative CaCC, TMEM16A. Isometric force, [Ca(2+)]i, and SMC membrane potential were measured in isolated arterial segments. I Cl(Ca) and GTPγS-induced nonselective cation current were measured in isolated SMCs. Downregulation of TMEM16A resulted in inhibition of both the cGMP-dependent I Cl(Ca) and the "classical" I Cl(Ca) in SMCs. TMEM16A downregulation also reduced expression of bestrophins. TMEM16A downregulation suppressed vasomotion both in vivo and in vitro. Downregulation of TMEM16A reduced agonist (noradrenaline and vasopressin) and K(+)-induced contractions. In accordance with the depolarizing role of CaCCs, TMEM16A downregulation suppressed agonist-induced depolarization and elevation in [Ca(2+)]i. Surprisingly, K(+)-induced depolarization was unchanged but Ca(2+) entry was reduced. We suggested that this is due to reduced expression of the L-type Ca(2+) channels, as observed at the mRNA level. Thus, the importance of TMEM16A for contraction is, at least in part, independent from membrane potential. This study demonstrates the significance of TMEM16A for two SMCs I Cl(Ca) and vascular function and suggests an interaction between TMEM16A and L-type Ca(2+) channels.
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