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Effects of superoxide anion on intracellular Ca2+ concentration in rabbit pulmonary arterial smooth muscle cells

  
@article{APS7358,
	author = {Yi-ping Wang and Masahiro Oike and Yushi Ito},
	title = {Effects of superoxide anion on intracellular Ca2+ concentration in rabbit pulmonary arterial smooth muscle cells},
	journal = {Acta Pharmacologica Sinica},
	volume = {20},
	number = {1},
	year = {2016},
	keywords = {},
	abstract = {AIM:
To study the effect of superoxide anion on the Ca2+ homeostasis in smooth muscle cells isolated from the rabbit pulmonary artery.
METHODS:
Intracellular Ca2+ concentration ([Ca2+]i) was investigated using cell suspension of freshly isolated smooth muscle cells from rabbit pulmonary artery (PASMC). Fura-2 fluorescent ratio obtained at 340 nm and 380 nm wave lengths was measured as an indicator of [Ca2+]i.
RESULTS:
ATP 30 mumol.L-1 induced a transient increase in the ratio (Ca2+ transient). Thapsigargin, an inhibitor of sarcoplasmic Ca2+ ATPase, induced a phasic increase in the ratio due to Ca2+ leak from intracellular store sites, but not the sustained increase, thereby suggesting the absence of Ca2+ release-activated Ca2+ entry (CRAC) mechanism in PASMC. When PASMC were exposed to superoxide anion by the pretreatment with xanthine and xanthine oxidase (X/XO) for 30 min, sustained component of ATP-induced Ca2+ transient was elevated. The ratios at 5 and 10 min after ATP application (delta ratio5 min and delta ratio10 min) were increased from 0.091 +/- 0.022 to 0.149 +/- 0.048 (P < 0.05) and from 0.021 +/- 0.020 to 0.117 +/- 0.047 (P < 0.01), respectively. But, thapsigargin-induced [Ca2+]i transient was not affected by X/XO.
CONCLUSION:
Superoxide anion makes ATP-induced Ca2+ transient sluggish, and does not affect Ca2+ leak pathway in PASMC.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/7358}
}