| Objective: To observe the change of the endothelium-dependent vasodilatation and serum antioxidants, free fatty acid in the patients with essential hypertension (EH) after acute glucose loading. To explore the relationship between these changes and insulin resistance, and the effects of different drug intervention.Methods: 52 essential hypertensive patients and 29 normal subjects were randomly divided into 3 groups. Glucose (Glu), insulin (INS), superoxide dismutase (SOD), total antioxide capacity (T-AOC), anti-superoxide anion free radical (Anti O2。—) and free fatty acid (FFA) in fasting serum were measured after a 12-hour overnight fast. The inner diameter of brachial artery was assessed by a high-resolution ultrasound system before and after reactive hyperemia. Endothelium-dependent flow-mediated dilation (EDF) was calculated as the percent change in brachial artery diameter 1 min after reactive hyperemia compared with baseline. Afterwards, all patients took the following glucose and/or drugs respectively: Glucose 75g (41 cases, EH 26 cases, NS 15 cases); Glucose 75g + V.C 2.0g + V.E 0.8g (20 cases, EH 13 cases, NS 7 cases); Glucose 75g + Metformin 0.5g (20 cases, EH 13 cases, NS 7 cases). The above mentioned parameters were repeatedly determined 1,2 and 3 hours after glucose loading.Results: (1) In the OGTT group, baseline EDF in essential hypertensive patients was significantly lower than that of the normal subjects (13.64±5.01% vs 17.43±5.66%,P<0.05). EDF in both EH and NS was impaired significantly (9.48 ± 3.33% vs 13.64 ± 5.01%,14.35 ± 5.86% vs 17.43 ± 5.66%,p<0.05) after acute glucose loading; furthermore this impairment in EH was more serious than that in NS (31.74 ± 6.91% vs 13.03 ± 5.94%,P<0.05). 42% (11/26 cases) EH with impaired EDF were found 1 hour after acute glucose loading. EDF in both EH and NS groups was restored 2 hours after eating glucose. (2) IR was observed in 17 cases of EH, with an incidence rate of 65%. 1 hour after taking glucose, EDF was impaired in 47% EH with insulin resistance (IR), 26% EH with normal insulin sensitivity (NIS), and 22% NS. (3) In both EH and NS of the OGTT group, EDF was impaired 1 hour after glucose loading, but there was no apparent change in the V.C + V.E group and the MF group. (4) No significant difference of fasting serum SOD, T-AOC, Anti O2。— concentration was observed between EH and NS in all groups. SOD in EH of the OGTT group was significantly decreased 1 hour after glucose loading compared to the baseline concentration (79.36 ± 10.58 vs 89.35 ± 19.34NU/ml,P<0.05). No significant difference in the V.C + V.E group and the MF group. T-AOC concentration was lower in EH than that in NS of the OGTT group (8.43 ± 2.82 vs 13.46 ± 4.31U/ml,P<0.05). The concentration of Anti O2。— in EH of the OGTT group significantly decreased compared with the baseline concentration (P<0.05) and lasted 3 hours, which in EH of the V.C + V.E group and the MF group was higher than that in EH of the OGTT group (256.30 ± 61.80,256.89 ± 72.16U/L vs 193.88 ± 47.87U/L,P<0.05). (5) The concentration of FFA in EH of the MF group decreased greatly 1 hour after glucose loading (108.14 ± 53.05 vs 236.55 ± 80.53μmol/L,P<0.05) and lasted 3 hours, which was significantly lower than that in EH of the OGTT group (108.14 ± 53.05 vs 200.56 ± 34.38μmol/L,P<0.05). (6) Multivariate analysis showed that EDF was negatively related to Glu 1 hour after OGTT, SBP, DBP, IS-AUC and BMI; and negatively related to ISI.Conclusion: 1. EDF in EH patients is transiently impaired after oral glucose loading. 2. Insulin resistance aggravates impairment which caused by hyperglycemia in EH patients. 3. The decreased antioxidative capacity and the increased FFA level may be one of the mechanisms. 4. The acute impaired EDF caused by hyperglycemia can be apparently attenuated by the co-administration of large dose antioxidant vitamin C and E or Metformin. |
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