| Backgrounds: It is thought highly that the origin and development of hypertension is closely associated with high level of glucocorticosteroid in the blood at present。Previously, it was considered that mineralocorticoid hormone lead to hypertension. The present study shows that Glucocorticoids (GC) inhibits inducible and constitutive nitric oxide synthase (NOS),GC also enhance generation of free radicals, in particular reactive oxygen species (ROS). N-acetylcysteine (NAC) is a water-soluble antioxidant,and the study has discovered NAC can reduce blood pressure in spontaneous hypertensive rat[1].Objective: In the present study, we examine the effects of Dexamethasone on SBP,ROS and NO to the change of hypertension, and approach its mechanism。It is more important that we try to ascertain whether NAC is helpful for Glucocorticoids inducing hypertension or not. The study will be a foundation for the further study in future.Methods:After adaptively fed for one week, Male Sprague-Dawley(SD) rats were randomly divided into four groups .Controls. Group 1– saline treatment (N = 10): First tap water refreshed for 4 days, then saline injection (1 ml/kg s.c.) daily at for further 9 days, Rats were given tap water to drink in the same time. Group 2–Dex treatment (N = 10): First tap water refreshed for 4 days, then injection of Dex(50μg/kg s.c.) daily at for further 9 days, rats were given tap water to drink in the same time. Group 3– NAC + saline (N = 10): NAC (10 g/L in the drinking water) refreshed daily for 4 days prior to and during coadministration with saline (1 ml/kg s.c.) daily for further 9 days. Group 4– NAC + Dex (N = 10): NAC (10 g/L in the drinking water) refreshed for 4 days prior to and during coadministration with Dex (50μg/kg s.c.) daily for further 9 days. SBP was measured at 10:00–11:00 hr on every day using a tail-cuff system. The animals were weighted on every day after SBP measurement. Animal drinking bottles were weighted daily to assess water consumption. Plasma NO was determined by the reduction of nitrate to nitrite using a modified Griess color reaction. Aortic Superoxide Production was measured using lucigenin enhanced chemiluminescence assay.Result: Group 1– saline injection of saline did not alter SBP (SBP 116.60±2.22mmHg T5, 115.00±3.13mmHg T13,P > 0.05). Group 2–Dex increased SBP from 117.50±1.65mmHg T5 to 129.40±2.55 mmHg T13 (P < 0.05). Group 3– NAC + saline prevention Pretreatment with NAC (10 g/L/dayin drinking water) had no effect on SBP (114.50±2.68mmHg T1 versus 115.40±3.13mmHg T4, ns). The combination of NAC and saline treatment did not alter SBP (116.60±2.22mmHg T5 versus 114.5±3.10mmHg T13,P > 0.05) . Group 4– NAC + Dex prevention Pretreatment with NAC did not alter SBP (114.90±1.79mmHg T1 and 115.30±1.57mmHg T4, ns). Subsequent Dex treatment increased SBP from 115.50±2.37mmHg T5 to 124.2±3.94mmHg T13, (P < 0.05). The SBP of SD rats in Group 2 was higher than the Group 4 after Dex treatment.Plasma NO concentration in Group 2 (15.62±3.50um/L) was lower than in the Group 1 (23.27±3.78um/L) (P < 0.01). Plasma NO concentration in Group 4 (16.37±3.01um/L) was lower than in the Group 3 (24.10±2.81 um/L) (P < 0.01). There was no significant difference in plasma NO between Group1and Group 3 (P >0.05). There was no significant difference in plasma NO between Group2 and Group 4 (P >0.05).Aortic superoxide production was higher in Group 2 (6851.24±462.72count/min·mg) than group 1 (3754.36±452.22count/ min·mg) (P < 0.01), higher in Group 4 (5784.36±598.23count/ min·mg) than Group 3 (3674.43±594.48 count/ min·mg)(P < 0.01), higher in Group 2 than Group 4 (P < 0.01), There was no significant difference in aortic superoxide production between Group1 and Group 3 (P >0.05).Conclusion: NAC (10g/L) can partially antagonize the development Dex-induced hypertension. Given its relative ineffectiveness, poor bioavailability, and potential toxicity in large dose, NAC is not a receivable candidate for solitary treatment of GC-hypertension in humans.
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