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• W1983194760 endingPage "H1747" @default.
• W1983194760 startingPage "H1741" @default.
• W1983194760 abstract "Rats submitted to high altitude (Cerro de Pasco, Perú, 4,340 m, Po 2 = 12.2 kPa) for up to 84 days showed a physiological adaptive response with decreased body weight gain (15%), increased right ventricle weight (100%), and increased hematocrit (40%) compared with sea level animals. These classical parameters of adaptation to high altitude were accompanied by an increase in heart mitochondrial enzymes: complexes I-III activity by 34% and mitochondrial nitric oxide synthase (mtNOS) activity and expression by >75%. The hyperbolic increase for mtNOS activity during adaptation to high altitude was similar to the observed pattern for hematocrit. Hematocrit and mtNOS activity mean values correlated linearly ( r 2 = 0.75, P ≤ 0.05). Chronic treatment for 28 days with sildenafil (50 mg·kg −1 ·day −1 ) decreased the response of mtNOS to high altitude by 25%. Conversely, N G -nitro-l-arginine methyl ester treatment (8.3 mg·kg −1 ·day −1 ) increased such response by 40%, whereas l-arginine treatment (106 mg·kg −1 ·day −1 ) had no effect. Nitric oxide (NO) production by mtNOS accounts for ∼49% of total cellular NO production in sea level rats and for ∼54% in rats exposed to high altitude for 84 days. It is concluded that mtNOS is a substantial source of cardiac NO, a factor in the adaptive response to sustained heart hypoxia that is susceptible to be modified by pharmacological treatments." @default.
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• W1983194760 date "2009-06-01" @default.
• W1983194760 modified "2023-09-25" @default.
• W1983194760 title "Mitochondrial nitric oxide metabolism during rat heart adaptation to high altitude: effect of sildenafil,<scp>l</scp>-NAME, and<scp>l</scp>-arginine treatments" @default.
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• W1983194760 doi "https://doi.org/10.1152/ajpheart.00422.2008" @default.
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