Suzuki Ryo, Fukuda Noboru, Katakawa Mayumi, Tsunemi Akiko, Tahira Yoshiko, Matsumoto Taro, Ueno Takahiro, Soma Masayoshi
Division of Nephrology Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Am J Hypertens. 2014 May;27(5):695-701. doi: 10.1093/ajh/hpt208. Epub 2013 Nov 7.
Endothelial progenitor cells (EPCs) induce neovascularization and repair vascular damage. We have demonstrated that EPC function is impaired in hypertensive rats with increases in oxidative stress and that angiotensin II receptor blockers improved the impaired function of EPCs. In this study, we investigated basal EPC functions in normotensive control subjects and patients with essential hypertension and the effect of losartan on EPC function in hypertensive patients.
Eighteen normotensive control subjects and 36 patients with essential hypertension who were undergoing treatment participated in the study. Hypertensive patients were randomly selected to receive 50mg of losartan or 4 mg of trichlormethiazide daily for 4 weeks. Peripheral blood mononuclear cells were isolated and cultured to assay EPC colony formation. Blood pressure, biological examination, and oxidative stress were evaluated in all subjects.
The number of EPC colonies was significantly lower in patients with essential hypertension than in normotensive control subjects. EPC colony number was significantly and inversely correlated with systolic and diastolic blood pressure in all subjects. EPC colony number was significantly increased by treatment with losartan in patients with essential hypertension but not affected by treatment with trichlormethiazide.
EPC function was inversely correlated with blood pressure and was impaired in essential hypertension. Losartan significantly improved the impaired EPC function in hypertensive patients. Impaired EPC function may determine the cardiovascular complications in essential hypertension. The improvement of EPC function with the administration of angiotensin II receptor blockers is considered to be one of the cardiovascular protective effects.
内皮祖细胞（EPCs）可诱导新血管形成并修复血管损伤。我们已经证明，在氧化应激增加的高血压大鼠中，EPC功能受损，并且血管紧张素II受体阻滞剂可改善EPC受损的功能。在本研究中，我们调查了血压正常的对照受试者和原发性高血压患者的基础EPC功能，以及氯沙坦对高血压患者EPC功能的影响。
18名血压正常的对照受试者和36名正在接受治疗的原发性高血压患者参与了本研究。高血压患者被随机选择，每天接受50mg氯沙坦或4mg三氯噻嗪治疗，持续4周。分离并培养外周血单核细胞以检测EPC集落形成。对所有受试者进行血压、生物学检查和氧化应激评估。
原发性高血压患者的EPC集落数量显著低于血压正常的对照受试者。在所有受试者中，EPC集落数量与收缩压和舒张压显著负相关。氯沙坦治疗可使原发性高血压患者的EPC集落数量显著增加，但三氯噻嗪治疗对其无影响。
EPC功能与血压呈负相关，在原发性高血压中受损。氯沙坦可显著改善高血压患者受损的EPC功能。EPC功能受损可能决定原发性高血压的心血管并发症。给予血管紧张素II受体阻滞剂改善EPC功能被认为是心血管保护作用之一。
