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J Smooth Muscle Res. 2018;54(0):71-82. doi: 10.1540/jsmr.54.71.

Role of calcium channels and endothelial factors in nickel induced aortic hypercontraction in Wistar rats.

Author information

1
Department of Biosciences, Jamia Millia Islamia, New Delhi 110025, India.

Abstract

AIM:

To investigate the mechanism of nickel augmented phenylephrine (PE)-induced contraction in isolated segments of Wistar rat aorta.

MATERIALS AND METHODS:

Effect 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.

RESULTS:

Endothelium 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.

CONCLUSION:

Nickel 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 Ca2+ channels in smooth muscle cells.

KEYWORDS:

Hypercontraction; L-type Ca2+ channels; Nickel; Reactive Oxygen Species; T-type Ca2+ channels

PMID:
30210089
PMCID:
PMC6135920
DOI:
10.1540/jsmr.54.71
[Indexed for MEDLINE]
Free PMC Article

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