Effects and Mechanisms of Tea Regulating Blood Pressure: Evidences and Promises

Abstract

Cardiovascular diseases have overtaken cancers as the number one cause of death. Hypertension is the most dangerous factor linked to deaths caused by cardiovascular diseases. Many researchers have reported that tea has anti-hypertensive effects in animals and humans. The aim of this review is to update the information on the anti-hypertensive effects of tea in human interventions and animal studies, and to summarize the underlying mechanisms, based on ex-vivo tissue and cell culture data. During recent years, an increasing number of human population studies have confirmed the beneficial effects of tea on hypertension. However, the optimal dose has not yet been established owing to differences in the extent of hypertension, and complicated social and genetic backgrounds of populations. Therefore, further large-scale investigations with longer terms of observation and tighter controls are needed to define optimal doses in subjects with varying degrees of hypertensive risk factors, and to determine differences in beneficial effects amongst diverse populations. Moreover, data from laboratory studies have shown that tea and its secondary metabolites have important roles in relaxing smooth muscle contraction, enhancing endothelial nitric oxide synthase activity, reducing vascular inflammation, inhibiting rennin activity, and anti-vascular oxidative stress. However, the exact molecular mechanisms of these activities remain to be elucidated.

Keywords: endothelial function; hypertension; inflammation; tea secondary metabolites.

Figure 1

The underlying mechanisms of tea regulating blood pressure using animal, tissue and cell line models. After intake or adding into cell cultures, tea and its bioactive ingredients can alter several blood pressure regulating processes, including ① alleviation of the oxidative stress and improvement of the endothelial function in the aortas in vivo; ② mitigation of the inflammation and amelioration of the endothelial function in the aortic epithelial cell lines in vitro; ③ suppression of contractile response and improvement of vasodilation in the aortic tissues in vitro; ④,⑤ inhibition of renal sympathetic nerve activity and amelioration of arterial baroreceptor. Abbreviation: SOD, superoxide dismutase; HO-1, heme oxygenase 1; NOX, NADPH oxidase; p-AKT, phosphorylated protein kinase B; p-eNOS, phosphorylated endothelial nitric oxide synthase; NO, nitric oxide; PI3 Kinase, phosphatidylinositol 3 kinase; IL6, Interleukin 6; TNFα, Tumor necrosis factor α; MCP-1, Monocyte chemotactic protein-1; ET-1, Endothelin-1; RSNA, renal sympathetic nerve activity.