Exercise has been proved to promote the number and activity of circulating endothelial progenitor cells (EPCs) in humans, which contributes to improvement in endothelial function and maintenance of cardiovascular homoeostasis. However, the mechanism underlying the effect of exercise on circulating EPCs in healthy subjects is not completely understood. Here, we investigated whether the regulation of acute exercise on circulating EPCs is associated with nitric oxide (NO), vascular endothelial growth factors (VEGF) and granulocyte macrophage colony stimulating factor (GM-CSF) known to modulate circulating EPCs in healthy subjects. A total of 16 healthy male volunteers underwent a modified Bruce treadmill acute exercise protocol. The number and activity of circulating EPCs, as well as the levels of NO-VEGF and GM-CSF in plasma and culture medium before and after exercise in healthy subjects were measured. The number and activity of circulating EPCs after acute exercise were significantly higher than those before exercise in healthy subjects. In parallel, acute exercise significantly enhanced plasma NO level in healthy subjects. There is a significant linear regression relationship between the enhanced plasma NO level and increased number or activity of circulating EPCs. However, no change of plasma VEGF and GM-CSF level was observed after acute exercise. The secretion of NO-VEGF and GM-CSF by cultured EPCs remained unchanged in response to acute exercise. The present study demonstrates for the first time that acute exercise-induced NO production contributes to upregulation of circulating EPCs in healthy subjects, which suggests that NO plays an important role in the regulation of exercise on circulating EPCs.

Vascular dysfunction in hypertensive condition is characterized by impaired endothelial function and reduced artery elasticity. Circulating endothelial microparticles (EMPs) and brachial-ankle pulse wave velocity (baPWV) are novel evaluation parameters for vascular function. However, their changes in patients with well-controlled blood pressure (BP) have not been fully acquired. To address this issue, circulating EMPs, defined as CD31 þ /CD42À MPs and baPWV were detected in 30 healthy subjects, 30 uncontrolled hypertensive (UCHT) patients and 23 well-controlled hypertensive (WCHT) patients. UCHT patients displayed elevated baPWV (Po0.01) and circulating EMPs (Po0.01) compared with healthy subjects. In WCHT patients, vascular damage represented by these two parameters constantly existed (Po0.01). Values of circulating EMPs were positively related to baPWV (Po0.01). Multivariate regression defined circulating EMPs as an independent contributor to the increase of baPWV value (Po0.05). Our study indicated that though BP was controlled, impaired endothelial function and arterial elasticity continued. The optimal therapy for patients with hypertension should include not only lowering BP but also improvement of vascular injury in parallel.

Berberine (BR) has been proved to promote endothelial function. However, the exact mechanisms underlying the effect of BR on endothelial function are not completely clear. It has been demonstrated that endothelial progenitor cells (EPCs) contribute to improvement of endothelial function and C2 small artery elasticity index is a surrogate parameter for the clinical evaluation of endothelial function. We hypothesized that BR-induced mobilization of circulating EPCs is associated with BR-related improvement of endothelial function. To address this assumption, 15 healthy volunteers were recruited and received BR 0.4 g three times per day for 30 days. The number of circulating CD34/KDR double-positive cells as well as C1 large and C2 small artery elasticity indices were evaluated before and after BR therapy. The number of CD34/KDR doublepositive EPCs increased significantly after BR treatment (0.030 ± 0.020% vs 0.017 ± 0.010%, Po0.01). After 30-day BR therapy C2 increased significantly (6.21±2.80 ml per mm Hg  100 vs 4.06±2.67 ml per mm Hg  100, Po0.01) and C1 remained unchanged (10.79 ± 3.27 ml per mm Hg  10 vs 10.06 ± 2.08 ml per mm Hg  10, P40.05). The increment of CD34/KDR double-positive EPCs was positively correlated with the increment of C2 (r ¼ 0.68, Po0.01). We concluded that BR-induced mobilization of circulating EPCs contributes to improvement of small artery elasticity in healthy persons.

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