ArticleJournal of molecular and cellular cardiology2015
Overexpression of ANO1/TMEM16A, an arterial Ca2+-activated Cl- channel, contributes to spontaneous hypertension.
Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 99 citations in OpenAlex.
- Renin-Angiotensin Signaling and Vascular Function: Insights into Health and Disease.Acta physiologica (Oxford, England) · 2026Review
- Loss of Vascular TMEM16A Impairs Cerebral Autoregulation and Exacerbates Ischemia-reperfusion Injury.Translational stroke research · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- CaActa physiologica (Oxford, England) · 2026Review
- TMEM16A in gastrointestinal and vascular smooth muscle contractility.The Journal of physiology · 2025Review
- The emerging role of anoctamin-1 in cardiac and cerebrovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- ANO1: central role and clinical significance in non-neoplastic and neoplastic diseases.Frontiers in immunology · 2025Review
- Function and Regulation of the Calcium-Activated Chloride Channel Anoctamin 1 (TMEM16A).Handbook of experimental pharmacology · 2024Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Chloride Ions, Vascular Function and Hypertension.Biomedicines · 2022Review
- Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022Review
- Downregulation of CaFrontiers in pharmacology · 2022Article
- Clues and new evidences in arterial hypertension: unmasking the role of the chloride anion.Pflugers Archiv : European journal of physiology · 2022Review
- Positive modulation of the TMEM16B mediated currents by TRPV4 antagonist.Biochemistry and biophysics reports · 2021Article
- 7,8-Dihydroxyflavone Enhanced Colonic Cholinergic Contraction and Relieved Loperamide-Induced Constipation in Rats.Digestive diseases and sciences · 2021Article
- Molecular mechanisms of activation and regulation of ANO1-Encoded CaChannels (Austin, Tex.) · 2021Review
- Role of Potassium Ions in Regulation of Calcium-Activated Chloride Channels.Doklady. Biochemistry and biophysics · 2021Article
- An outer-pore gate modulates the pharmacology of the TMEM16A channel.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- 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
- Emerging Modulators of TMEM16A and Their Therapeutic Potential.The Journal of membrane biology · 2021Review
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4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium-activated chloride channels (CaCCs) have been implicated in hypertension; however, the mechanism underlying their involvement is unknown. The aim of this study was to determine whether the CaCC ANO1 is involved in the pathogenesis of spontaneous hypertension. Arterial ANO1 expression and the effects on blood pressure (BP) of inhibiting ANO1 with an ANO1 inhibitor, T16(Ainh)-A01, and in vivo RNAi, were examined in spontaneously hypertensive rats (SHRs). Knockdown of ANO1 by siRNA prevented hypertensive development, and attenuation of ANO1 channel activity reduced BP in SHRs. Angiotensin II upregulated ANO1 expression in primary cultures of vascular smooth muscle cells (VSMCs). The protein level and activity of cellular ANO1 positively correlated with VSMC proliferation. Our data indicate an important role of increased ANO1 expression and activity in inducing hypertension in SHRs. It may mediate angiotensin II-dependent vascular remodeling. Our results increase the mechanistic understanding of hypertension and suggest ANO1 as a possible therapeutic target for hypertension.
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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.