Blood pressure reduction due to hemoglobin glycosylation in type 2 diabetic patients.
Blood pressure reduction due to hemoglobin glycosylation in type 2 diabetic patients.
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DOI：
10.2147/vhrm.s3077
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发表时间：
2008
影响因子：
2.9
通讯作者：
Guerrero-Romeros F
中科院分区：
文献类型：
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作者：
Cabrales P;Salazar Vázquez MA;Salazar Vázquez B;Rodríguez-Morán M;Intaglietta M;Guerrero-Romeros F
验证血红蛋白糖基化是高血压危险因素的假设。共有129名相对统一的糖尿病受试者（86名女性和42名男性）参加了一项横断面研究。排除标准包括饮酒、吸烟、缺血性心脏病、中风、肿瘤、肾脏、肝脏和慢性炎症性疾病。在随后的几天中记录收缩压和舒张压，并测定平均动脉血压（MAP）。通过自动化微粒子酶免疫测定试验测定糖化血红蛋白（HbA 1c）百分比，测量血红蛋白糖化。发现MAP与HbA 1c浓度无关;然而，当从分析中排除接受高血压治疗的患者时，根据红细胞压积的变异性校正MAP，以证明血管收缩（或血管舒张）的水平，表明MAP与HbA 1c浓度呈负相关（趋势p <0.05）。接受高血压治疗的患者显示出相反的趋势，随着HbA 1c的增加，MAP增加（趋势差异p <0.05）。糖基化本身似乎导致未治疗高血压的2型糖尿病患者血压降低。高血压治疗可能与内皮功能障碍水平相关，该水平会干扰HbA 1c的降压作用。
To test the hypothesis that glycosylation of hemoglobin constitutes a risk factor for hypertension. A total of 129 relative uniform diabetic subjects (86 women and 42 men) were enrolled in a cross sectional study. Exclusion criteria included alcohol consumption, smoking, ischemic heart disease, stroke, neoplasia, renal, hepatic, and chronic inflammatory disease. Systolic and diastolic pressures were recorded in subsequent days and mean arterial blood pressure (MAP) was determined. Hemoglobin glycosylation was measured by determining the percentage glycosylated hemoglobin (HbA1c) by means of the automated microparticle enzyme immunoassay test. MAP was found to be independent of the concentration of HbA1c; however, correcting MAP for the variability in hematocrit, to evidence the level of vasoconstriction (or vasodilatation) showed that MAP is negatively correlated with the concentration of HbA1c (p for trend <0.05), when patients treated for hypertension are excluded from the analysis. Patients treated for hypertension showed the opposite trend with increasing MAP as HbA1c increased (p for the difference in trends <0.05). Glycosylation per se appears to lead to blood pressure reduction in type 2 diabetic patients untreated for hypertension. Treatment for hypertension may be associated with a level of endothelial dysfunction that interferes with the antihypertensive effect of HbA1c.