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Review
. 2017 Aug 2;4:36.
doi: 10.3389/fnut.2017.00036. eCollection 2017.

Cocoa, Blood Pressure, and Vascular Function

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Free PMC article
Review

Cocoa, Blood Pressure, and Vascular Function

Valeria Ludovici et al. Front Nutr. .
Free PMC article

Abstract

Cardiovascular disease (CVD) represents the most common cause of death worldwide. The consumption of natural polyphenol-rich foods, and cocoa in particular, has been related to a reduced risk of CVD, including coronary heart disease and stroke. Intervention studies strongly suggest that cocoa exerts a beneficial impact on cardiovascular health, through the reduction of blood pressure (BP), improvement of vascular function, modulation of lipid and glucose metabolism, and reduction of platelet aggregation. These potentially beneficial effects have been shown in healthy subjects as well as in patients with risk factors (arterial hypertension, diabetes, and smoking) or established CVD (coronary heart disease or heart failure). Several potential mechanisms are supposed to be responsible for the positive effect of cocoa; among them activation of nitric oxide (NO) synthase, increased bioavailability of NO as well as antioxidant, and anti-inflammatory properties. It is the aim of this review to summarize the findings of cocoa and chocolate on BP and vascular function.

Keywords: arterial stiffness; blood pressure; cocoa; endothelial function; flavonoids.

Figures

Figure 1
Figure 1
Cocoa flavanols and endothelial function. ACE, angiotensin-converting enzyme; A I, angiotensin I; A II, angiotensin II; ECE, endothelin-converting enzyme; ET 1, endothelin-1; EDHF, endothelium-derived hyperpolarizing factor; eNOS, endothelial NO synthase; l-NAME, l-nitroarginine methyl ester; ROS, reactive oxygen species; NO, nitric oxide; cGMP, cyclic guanosine monophosphate; cAMP, cyclic adenosine monophosphate; COX, cyclooxygenase; PGI2, prostacyclin; TXA2, thromboxane A2; SOD, superoxide dismutase; CF, cocoa flavanol. CFs improve endothelial function via different pathways. They increase NO availability, stimulating eNOS function, preventing l-NAME-induced hypertension, and reducing ROS. They also stimulate EDHF-mediated relaxation, inhibit endothelin-1, and reduce ACE activity. Modified by Corti et al., Circulation 2009.

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