ArticleJournal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi2018
Role of calcium channels and endothelial factors in nickel induced aortic hypercontraction in Wistar rats.
Article in Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Characterization of calcium sources and downstream signaling pathways following electrical field stimulation of rodent longitudinal esophageal muscle.Frontiers in physiology · 2026Article
- Sex-specific modulation of T-type voltage-gated calcium channels in the renal artery of hypertensive rats.Frontiers in physiology · 2026Article
- Quercetin and resveratrol ameliorate nickel-mediated hypercontraction in isolated Wistar rat aorta.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2022Article
- Kinetic mechanisms by which nickel alters the calcium (CaJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the mechanism of nickel augmented phenylephrine (PE)-induced contraction in isolated segments of Wistar rat aorta. MATERIALS AND
methodsEffect of varying concentrations of nickel on PE-induced contraction were investigated in isolated segments of Wistar rat aorta using an organ bath system. Aortic rings were pre-incubated with verapamil (1 µM and 20 µM), gadolinium, apocynin, indomethacin or N-G-nitro-L-arginine methyl ester (L-NAME) separately before incubation with nickel.
resultsEndothelium intact aortic rings incubated with 100 nM, 1 µM or 100 µM of nickel exhibited 80%, 43% and 28% increase in PE-induced contraction, respectively, while no such enhancing responses were observed in endothelium denuded aorta. Incubation of aortic rings with 1 µM and 20 µM verapamil suggested an involvement of influx of calcium through T-type calcium channels in smooth muscle cells, while aortic rings pre-incubated with gadolinium showed no role of store operated calcium channels in the nickel effect on PE-induced contractions. The enhancing effect of nickel on PE-induced contractions was inhibited by apocynin, indomethacin or L-NAME.
conclusionNickel has caused augmentation of PE-induced contractions as a result of the endothelial generation of reactive oxygen species (ROS) and cyclooxygenase 2 (COX2) dependent endothelium contracting factors (EDCFs), which increases the influx of extracellular calcium through T-type Ca
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