Abstract

(1) Background: Endothelial dysfunction predicts cardiovascular events. Circulating angiogenic cells (CACs) maintain and repair the endothelium regulating its function. Tea flavonoids reduce cardiovascular risk. We investigated the effects of black tea on the number of CACs and on flow-mediated dilation (FMD) before and after an oral fat in hypertensives; (2) Methods: In a randomized, double-blind, controlled, cross-over study, 19 patients were assigned to black tea (150 mg polyphenols) or a placebo twice a day for eight days. Measurements were obtained in a fasted state and after consuming whipping cream, and FMD was measured at baseline and after consumption of the products; (3) Results: Compared with the placebo, black tea ingestion increased functionally active CACs (36 ± 22 vs. 56 ± 21 cells per high-power field; p = 0.006) and FMD (5.0% ± 0.3% vs. 6.6% ± 0.3%, p < 0.0001). Tea further increased FMD 1, 2, 3, and 4 h after consumption, with maximal response 2 h after intake (p < 0.0001). Fat challenge decreased FMD, while tea consumption counteracted FMD impairment (p < 0.0001); (4) Conclusions: We demonstrated the vascular protective properties of black tea by increasing the number of CACs and preventing endothelial dysfunction induced by acute oral fat load in hypertensive patients. Considering that tea is the most consumed beverage after water, our findings are of clinical relevance and interest.

Highlights

  • Hypertension is the leading risk factor for cardiovascular morbidity and mortality [1]

  • Recent studies have shown that risk factors for vascular diseases are associated with a blunted capacity for repair of the endothelial damage evidenced by a dysfunction of bone marrow-derived circulating endothelial progenitor cells (EPCs) [10]

  • In grade I hypertensive patients, one-week consumption of black tea resulted in a significant improvement in endothelium-dependent flow-mediated dilation (FMD), with maximal response two hours after acute intake

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Summary

Introduction

Hypertension is the leading risk factor for cardiovascular morbidity and mortality [1]. Recent studies have shown that risk factors for vascular diseases are associated with a blunted capacity for repair of the endothelial damage evidenced by a dysfunction of bone marrow-derived circulating endothelial progenitor cells (EPCs) [10]. A reduced ability of EPCs to proliferate ex vivo and to express an endothelial phenotype is associated with risk factors for coronary artery disease as well as endothelial dysfunction [10,11]. Cells grown under these conditions were formerly termed “early EPCs”, but are currently referred to as “circulating angiogenic cells”

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