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- W1501821610 abstract "Clinical use of nitroglycerin (GTN) is limited because its long-term therapy results in the development of nitrate tolerance. The etiology of nitrate tolerance is controversial and poorly understood. This study aimed to investigate the mechanisms of GTN-induced tolerance and to compare them in aorta and vena cava from GTN tolerant rats. In vivo tolerance for GTN was induced by 3 days treatment with GTN (150 mg/kg/day). We evaluated the maximum relaxing effect (ME) and the potency (pD2) induced by GNT in aorta and vena cava from tolerant and control rats. The endothelial NOS3 and soluble guanylyl-cyclase (sGC) protein expression was accessed by Western Blot. The procedures are according to the Ethics Committee. Differences were considered significant for P<0.05. GTN treatment reduced the pD2 of GTN from 14.3±0.8, n=6 to 12.8±0.6, n=6, whereas ME was not different between control and tolerant rat aorta. In vena cava, ME was lower in tolerant rats (35.2 ± 2.5%, n= 6, P<0.05) as compared to control rats (73.1 ± 5.7%, n=6). sGC expression was similar in aorta and vein from control and tolerant rats. However, NOS3 expression was higher in aortas from tolerant (1.08 ± 0.06 n= 6, P<0.05) than in control animals (0.66 ± 0.04, n=7). Similarly, NOS3 expression was higher in veins from tolerant (1.08 ± 0.06 n= 6, P<0.05) than in control animals (0.66 ± 0, 04, n= 7). Therefore, GTN-induced tolerance in rat aorta and vein involves NOS3 but not sGC." @default.
- W1501821610 created "2016-06-24" @default.
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- W1501821610 date "2015-04-01" @default.
- W1501821610 modified "2023-09-27" @default.
- W1501821610 title "Nitroglycerin‐induced tolerance in rat conduit artery and vein" @default.
- W1501821610 doi "https://doi.org/10.1096/fasebj.29.1_supplement.1052.1" @default.
- W1501821610 hasPublicationYear "2015" @default.
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