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目的探讨钠、钾干预在盐敏感性高血压的血压调控,循环和靶器官氧化应激损伤中的作用。方法以Dahl盐敏感性(DS)和SS-13BN(13BN)大鼠为动物模型,24只DS大鼠随机分为低盐组、高盐组、高盐补钾组、高盐+抗氧化剂(Tempol)组,每组6只;18只13BN大鼠随机分为低盐组、高盐组、高盐补钾组,每组6只。观察各组大鼠高盐、补钾和抗氧化干预4周后,血压、循环和肾髓质氧化应激水平的变化及烟酰胺腺嘌呤二核苷酸磷酸[NAD(P)H]氧化酶p22phox亚基表达的改变。结果与低盐组比较,高盐组干预后收缩压[DS:(169.92±2.17)比(147.12±6.09)mm Hg;13BN:(145.58±1.86)比(140.15±3.72)mm Hg]和血清丙二醛[DS:(20.11±2.19)比(15.56±0.52)μmol/L;13BN:(6.86±0.79)比(5.86±0.43)μmol/L]增高(均P<0.05)。DS大鼠中,与低盐组比较,高盐组血清总超氧化物歧化酶(SOD)活力降低[(4.05±0.35)×103比(4.90±0.24)×103 U/mL],补钾和抗氧化剂后增高[(6.13±0.16)×103、(5.46±0.32)×103比(4.05±0.35)×103 U/mL];肾髓质总SOD活力增高[(10.49±0.87)×10-2比(5.70±0.69)×10-2 U/mg pro],补钾和抗氧化剂后降低[(6.54±0.81)×10-2、(4.62±0.32)×10-2比(10.49±0.87)×10-2 U/mg pro];肾髓质丙二醛增高[(3.56±1.49)×102比(3.23±0.69)×102 nmol/mg pro],补钾后增高[(3.93±0.98)×102比(3.56±1.49)×102 nmol/mg pro];肾髓质p22phox蛋白表达增高[(10.48±4.96)比(1.63±1.03),P<0.05],补钾和抗氧化剂后降低[(5.59±4.12)、(8.01±3.70)比(10.48±4.96)](均P<0.05)。结论高盐可增强DS大鼠循环和肾髓质氧化应激水平,补钾和抗氧化剂均可拮抗其影响。
Objective To investigate the effects of sodium and potassium on blood pressure regulation, circulation and target organ oxidative stress in salt-sensitive hypertension. Methods Dahl’s salt-sensitive (DS) and SS-13BN (13BN) rats were used as experimental animal models. Twenty-four DS rats were randomly divided into low salt group, high salt group, high salt potassium group, Tempol group with 6 rats in each group. Eighteen 13BN rats were randomly divided into low salt group, high salt group and high salt potassium group, with 6 rats in each group. The changes of blood pressure, circulation and renal medullary oxidative stress were observed after high-salt, potassium and antioxidant intervention for 4 weeks in each group, and the changes of nicotinamide adenine dinucleotide phosphate [NAD (P) H] oxidase Changes in p22phox subunit expression. Results Compared with the low-salt group, the systolic blood pressure (SD) was significantly higher in the high-salt group after the intervention (DS: 169.92 ± 2.17 vs 147.12 ± 6.09 mm Hg; 145 ± 138 ± 1.86, 140.15 ± 3.72 mmHg) The dialdehyde levels were significantly higher in the control group than those in the control group (DS: (20.11 ± 2.19) vs (15.56 ± 0.52) μmol / L, and 13BN: (6.86 ± 0.79) vs (5.86 ± 0.43) μmol / L, respectively. Compared with the low-salt group, the serum total superoxide dismutase (SOD) in DS group decreased (4.05 ± 0.35) × 103 (4.90 ± 0.24) × 103 U / mL] (6.13 ± 0.16) × 103, (5.46 ± 0.32) × 103 (4.05 ± 0.35) × 103 U / mL], and the activity of SOD in renal medulla increased [(10.49 ± 0.87) × 10-2 (6.54 ± 0.81) × 10-2, (4.62 ± 0.32) × 10-2 (10.49 ± 0.87) × (5.70 ± 0.69) × 10-2 U / mg pro] (3.56 ± 1.49) × 102 (3.23 ± 0.69) × 102 nmol / mg pro], increased after potassium supplement [(3.93 ± 0.98) × 102 (3.56 ± 1.49) × 102 nmol / mg pro]; p22phox protein expression in renal medulla increased [(10.48 ± 4.96) vs (1.63 ± 1.03), P <0.05] 4.12), (8.01 ± 3.70) vs (10.48 ± 4.96) (all P <0.05). Conclusion High salt can increase the level of circulating oxidative stress and renal medulla in DS rats, both potassium and antioxidants can antagonize its effects.