ArticleJournal of vascular research2011
Angiotensin II upregulates Ca(V)1.2 protein expression in cultured arteries via endothelial H(2)O(2) production.
Article in Journal of vascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Calcium Signaling Pathway Genes RUNX2 and CACNA1C Are Associated With Calcific Aortic Valve Disease.Circulation. Cardiovascular genetics · 2015Trial
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- LncRNA ENSMUST00000155383 is Involved in the Improvement of DPP-4 Inhibitor MK-626 on Vascular Endothelial Function by Modulating Cacna1c-Mediated CaFrontiers in molecular biosciences · 2021Article
- 17β-estradiol reduces CaPharmacology research & perspectives · 2017Article
- Markers and Biomarkers of Endothelium: When Something Is Rotten in the State.Oxidative medicine and cellular longevity · 2017Review
- Effect of angiotensin II-induced arterial hypertension on the voltage-dependent contractions of mouse arteries.Pflugers Archiv : European journal of physiology · 2016Article
- Mineralocorticoid-receptor signalling in vascular smooth muscle.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2013Review
- Direct regulation of blood pressure by smooth muscle cell mineralocorticoid receptors.Nature medicine · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe previously reported that angiotensin II caused an endothelial-dependent increase in L-type voltage-dependent Ca(2+) channel (Ca(V)1.2) in cultured arteries, but the signaling pathways are not clear.
methodsEndothelial damage was generated by brief intra-arterial perfusion with 0.3% CHAPS. Ca(V)1.2 expression, function and H(2)O(2) were measured by Western blot, tension recording and Amplex Red H(2)O(2) assay kit, respectively.
resultsAngiotensin II dose-dependently upregulated Ca(V)1.2 expression in endothelium-intact arteries. The angiotensin II upregulation of Ca(V)1.2 expression in endothelium-intact arteries was blocked by NAD(P)H oxidase inhibitor diphenyleneiodonium (DPI), apocynin, a more specific NAD(P)H oxidase inhibitor gp91ds-tat and also by catalase. H(2)O(2) similarly upregulated Ca(V)1.2 expression in endothelium-intact and endothelium-damaged arteries, and the latter effect was also blocked by DPI and apocynin. Angiotensin II increased H(2)O(2) production by endothelium-intact but not by endothelium-damaged arteries, and this effect was blocked by apocynin, catalase and gp91ds-tat. The upregulation of Ca(V)1.2 by angiotensin II and H(2)O(2) is accompanied by an increased tension response to KCl and the Ca(2+) channel activator FPL 64176, and this effect was also attenuated by gp91ds-tat.
conclusionThese results suggest that angiotensin II stimulates endothelial NAD(P)H oxidase-produced H(2)O(2,) which may additionally act through vascular smooth muscle NAD(P)H oxidase, to upregulate vascular Ca(V)1.2 protein.
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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 Socratic graph.