Effects of mitochondrial L-arginine/nitric oxide system on mitochondrial Ca2+ transport in rat myocardium.
- Author:
Jun CAO
1
;
Yan-Rong SHI
;
Yong-Fen QI
;
Yong-Zheng PANG
;
Chao-Shu TANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Arginine; metabolism; Biological Transport; Calcium; metabolism; Female; Male; Mitochondria, Heart; metabolism; Myocytes, Cardiac; metabolism; Nitric Oxide; metabolism; Nitric Oxide Synthase; metabolism; Rats; Rats, Wistar
- From: Chinese Journal of Applied Physiology 2002;18(1):51-54
- CountryChina
- Language:Chinese
-
Abstract:
AIM AND METHODSTo observe the effect of myocardial mitochondrial L-arginine (L-Arg)/nitric oxide (NO) system on mitochondrial Ca2+ transport by using purified rat mitochondria and incubation of them in vitro.
RESULTSCompared with control group, incubation of mitochondria with L-Arg (10(-4) mol/L, NO substrate) or sodium nitroprusside (5 x 10(-7) mol/L, the donor of exogenous NO, SNP) increased significantly mitochondrial NO2- (66% and 89%, P < 0.01), respectively, and decreased the Ca2+ content (40% and 54%, P < 0.01). After L-Arg or SNP treatment, mitochondrial Ca2+ uptake were decreased by 67% and 85%, respectively (P < 0.01), vs control. The rate of mitochondrial Ca2+ release decreased by 11% and 8%, respectively (P < 0.01). When L-NAME (NO synthase inhibitor) was incubated with mitochondria and the L-Arg together, it inhibited the effects of L-Arg, NO2 on the mitochondrial NO2 formation, Ca2+ content descending, and decrease of Ca2+ uptake and release.
CONCLUSIONThe data suggest that myocardial mitochondrial L-Arg /NO systems take part in the regulation of cardiomyocytes Ca2+ transportation.
