ArticleThe Journal of pharmacology and experimental therapeutics2009
Molecular pharmacology of human Cav3.2 T-type Ca2+ channels: block by antihypertensives, antiarrhythmics, and their analogs.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Calcium channelopathies and intellectual disability: a systematic review.Orphanet journal of rare diseases · 2021Pooled it
- Calcium signaling pathway implicates a shared genetic basis between psychiatric and cardiovascular diseases.Translational psychiatry · 2026Article
- Upregulation of T-type voltage-dependent Ca²⁺ channels in activated hepatic stellate cells promotes liver fibrosis in metabolic dysfunction-associated steatohepatitis.Pflugers Archiv : European journal of physiology · 2026Article
- Inhibition of CaV1.4 channels by CaV3 channel antagonists ML218 and Z944.The Journal of general physiology · 2026Article
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- A non-conducting role of the CaeLife · 2024Article
- A non-conducting role of the CabioRxiv : the preprint server for biology · 2024Article
- Structural basis for human CaCell research · 2024Article
- Electric field stimulation unmasks a subtle role for T-type calcium channels in regulating lymphatic contraction.Scientific reports · 2023Article
- Electric field stimulation unmasks a subtle role for T-type calcium channels in regulating lymphatic contraction.Research square · 2023Article
- T-Type Calcium Channels: A Mixed Blessing.International journal of molecular sciences · 2022Review
- Propagation of Pacemaker Activity and Peristaltic Contractions in the Mouse Renal Pelvis Rely on CaFunction (Oxford, England) · 2022Article
- Mibefradil alters intracellular calcium concentration by activation of phospholipase C and IPMolecular biomedicine · 2021Article
- Cerebrovascular and neurological perspectives on adrenoceptor and calcium channel modulating pharmacotherapies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Review
- Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Pathophysiological roles and therapeutic potential of voltage-gated ion channels (VGICs) in pain associated with herpesvirus infection.Cell & bioscience · 2020Review
- High-content phenotypic assay for proliferation of human iPSC-derived cardiomyocytes identifies L-type calcium channels as targets.Journal of molecular and cellular cardiology · 2019Article
- A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism.Nature genetics · 2018Article
- T-type voltage-gated CaPharmacology research & perspectives · 2017Article
- CaEpilepsia · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Antihypertensive drugs of the "calcium channel blocker" or "calcium antagonist" class have been used to establish the physiological role of L-type Ca(2+) channels in vascular smooth muscle. In contrast, there has been limited progress on the pharmacology T-type Ca(2+) channels. T-type channels play a role in cardiac pacemaking, aldosterone secretion, and renal hemodynamics, leading to the hypothesis that mixed T- and L-type blockers may have therapeutic advantages over selective L-type blockers. The goal of this study was to identify compounds that block the Ca(v)3.2 T-type channel with high affinity, focusing on two classes of compounds: phenylalkylamines (e.g., mibefradil) and dihydropyridines (e.g., efonidipine). Compounds were tested using a validated Ca(2+) influx assay into a cell line expressing recombinant Ca(v)3.2 channels. This study identified four clinically approved antihypertensive drugs (efonidipine, felodipine, isradipine, and nitrendipine) as potent T-channel blockers (IC(50) < 3 microM). In contrast, other widely prescribed dihydropyridines, such as amlodipine and nifedipine, were 10-fold less potent, making them a more appropriate choice in research studies on the role of L-type currents. In summary, the present results support the notion that many available antihypertensive drugs block a substantial fraction of T-current at therapeutically relevant concentrations, contributing to their mechanism of action.
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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.