Relationship between Alteration of Circulating Endothelial Progenitor Cells and Arterial Elasticity in Patients with Essential Hypertension[J]. Journal of Sun Yat-sen University (Medical Sciences), 2012, 33(1).
Relationship between Alteration of Circulating Endothelial Progenitor Cells and Arterial Elasticity in Patients with Essential Hypertension[J]. Journal of Sun Yat-sen University (Medical Sciences), 2012, 33(1).DOI:
【Objective】 The study was to investigate the association between alteration in circulating endothelial progenitor cells (EPC) and hypertension-related reduced arterial elasticity. 【Methods】 We measured the artery elasticity profiles including C1 large and C2 small artery elasticity indices in the patients with essential hypertension (n=20) and age-matched normotensive subjects (n=21). We also performed flow cytometry analysis to evaluate the number of CD34 and KDR double-positive labeled circulating EPC before and after exercise
and acetylated-LDL and lectin fluorescent staining method to evaluate the number of cultured EPC. In addition
the EPC migratory and proliferative activities were measured. 【Results】 Compared with normotensive subjects
the patients with hypertension exhibited decreased C1 large and C2 small artery elasticity indices. The number of circulating EPC was not different between the two groups. The migratory and proliferative activities of circulating EPC in hypertensive patients were lower than those in normotensive subjects. Both proliferatory and migratory activities of circulating EPC closely correlated with C1 large and C2 small artery elasticity indices. Multivariate analysis identified both proliferative and migratory activities of circulating EPC as independent predictors of C1 large and C2 small artery elasticity indices. 【Conclusion】 The present study demonstrates for the first time that impaired activity of circulating EPC is associated with reduced arterial elasticity in patients with hypertension. The fall in endogenous repair capacity of vascular endothelium may be an important mechanism underlying hypertension-related vascular injury.