ArticlePflugers Archiv : European journal of physiology2014
T-type Ca(2+) channels facilitate NO-formation, vasodilatation and NO-mediated modulation of blood pressure.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- The role of T-type calcium channels in elderly human vascular function: A pilot randomized controlled trial.Experimental physiology · 2024Trial
- Albuminuria is associated with an increased prostasin in urine while aldosterone has no direct effect on urine and kidney tissue abundance of prostasin.Pflugers Archiv : European journal of physiology · 2017Trial
- Differential contribution of T-type voltage-gated calcium channels to vascular reactivity in the aorta and renal artery of healthy rabbits.Experimental physiology · 2026Article
- Sex-specific modulation of T-type voltage-gated calcium channels in the renal artery of hypertensive rats.Frontiers in physiology · 2026Article
- Treating Metabolic Dysregulation and Senescence by Caloric Restriction: Killing Two Birds with One Stone?Antioxidants (Basel, Switzerland) · 2025Review
- Can a pill (CaExperimental physiology · 2024Article
- Histamine HPflugers Archiv : European journal of physiology · 2024Article
- CaScientific reports · 2023Article
- Adipocyte-Endothelium Crosstalk in Obesity.Frontiers in endocrinology · 2021Review
- Ion-Channel modulator TH1177 reduces glomerular injury and serum creatinine in chronic mesangial proliferative disease in rats.BMC nephrology · 2020Article
- Deficiency of T-type voltage-gated calcium channels results in attenuated weight gain and improved endothelium-dependent dilatation of resistance vessels induced by a high-fat diet in mice.Journal of physiology and biochemistry · 2020Article
- Deletion of T-type calcium channels CaPflugers Archiv : European journal of physiology · 2018Article
- Contribution of S4 segments and S4-S5 linkers to the low-voltage activation properties of T-type CaV3.3 channels.PloS one · 2018Article
- Endothelial mineralocorticoid receptor ablation does not alter blood pressure, kidney function or renal vessel contractility.PloS one · 2018Article
- Direct activation of CaEuropean journal of pharmacology · 2017Article
- T-type CaChannels (Austin, Tex.) · 2017Review
- Article
- Age-dependent impact of CaThe Journal of physiology · 2016Article
- Nox1 upregulates the function of vascular T-type calcium channels following chronic nitric oxide deficit.Pflugers Archiv : European journal of physiology · 2015Article
- Ca(V)3.2 channels and the induction of negative feedback in cerebral arteries.Circulation research · 2014Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated calcium channels are involved in the vascular excitation-contraction mechanism and regulation of arterial blood pressure. It was hypothesized that T-type channels promote formation of nitric oxide from the endothelium. The present experiments determine the involvement of T-type channels in depolarization-dependent dilatation of mesenteric arteries and blood pressure regulation in Cav3.1 knock-out mice. Nitric oxide-dependent vasodilatation following depolarization-mediated vasoconstriction was reduced significantly in mesenteric arteries from Cav3.1(-/-) compared to wild type mice. Four days of systemic infusion of a nitric oxide (NO)-synthase-inhibitor to conscious wild type elicited a significant increase in mean arterial blood pressure that was absent in Cav3.1(-/-) mice. Immunoprecipitation and immunofluorescence labeling showed co-localization of Cav3.1 and endothelial nitric oxide synthase (eNOS) in arteries from wild type mice. Nitric oxide release measured as DAF fluorescence and cGMP levels were significantly lower in depolarized Cav3.1(-/-) compared to wild type arteries. In summary, the absence of T-type Cav3.1 channels attenuates NO-dependent dilatation in mesenteric arteries in vitro, as well as the hypertension after L-NAME infusion in vivo. Furthermore, Cav3.1 channels cluster with eNOS and promote formation of nitric oxide by the endothelium. The present findings suggest that this mechanism is important for the systemic impact of NO on peripheral resistance.
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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.