A large body of evidence supports that the dietary intake of polyphenols - particularly of flavonoids and the specific class of flavonoids named flavanols - might be able to exert some beneficial vascular effects and reduce the risk for cardiovascular morbidity and mortality. The review of epidemiological and mechanistic studies supports the role of flavonoids, particularly cocoa and tea flavanols, in protecting the cardiovascular system against cardiovascular disease. Nevertheless, flavonoids are an heterogeneous group of natural molecules differently represented in fruit and vegetables and definitive data on cardiovascular benefits are lacking. The weakness of the available data include few and very small studies, no crossover designed studies and a wide range of dose and type of flavonoids tested. Thus, although flavonoid-rich foods and beverages are likely to protect cardiovascular system, further research is needed to characterize the mechanism of action on flavanol-rich foods. Long-term clinical trials are also needed to definitively clarify the benefits deriving from long-term consumption of flavanol-rich foods, particularly focussing on the lowest effective levels as well as synergism or antagonistic actions between different classes of flavonoids commonly found in foods.

Epidemiological evidence supports the concept that diets rich in fruits and vegetables promote health and attenuate or delay the onset of cardiovascular disease (CVD). Although a variety of factors contribute to the beneficial effects of plant foods, much attention has been addressed to plant polyphenols. In this regard, in the daily Western diet, both black and green teas contribute to a relevant proportion of total phenol intake. The more abundant class of flavonoids that is present in teas is represented by flavanols, i.e., catechin, epicatechin, epigallocatechin, epicatechin gallate, and epigallocatechin gallate. Studies using animal models of atherosclerosis indicate that dietary flavonoid consumption delays atherosclerotic plaque development. Accordingly, an inverse association between tea intake and CVD has been demonstrated. Further, flavonoids can reduce endothelial dysfunction, i.e., the key step in the development of atherosclerosis. Concordantly, human data suggest that tea may reduce blood pressure levels. Despite this, although they often show that tea may have cardiovascular protective effects, results from epidemiological studies exploring the association between tea and health are controversial. Conflicting results may be caused by disparate study designs and flavonoid contents in different kinds of tea. Thus, because tea is a popular beverage worldwide, and several studies have shown that it is protective against CVD, further studies are needed to determine the role of tea in primary and secondary cardiovascular prevention.

Our findings highlight the important role played by an endothelium/NO-mechanism in the regulation of basal tone and in both mediating vasorelaxation and counteracting vasoconstriction induced by low concentrations of flavanols in rat thoracic aorta.

The role of the tachykinin neurokinin (NK)(2) receptors on rabbit distal colon propulsion was investigated by using two selective NK(2)-receptor antagonists, MEN-10627 and SR-48968. Experiments on colonic circular muscle strips showed that contractile responses to [beta-Ala(8)]NKA-(4-10) (1 nM-1 microM), a selective NK(2)-receptor agonist, were competitively antagonized by MEN-10627 (1-100 nM), whereas SR-48968 (0.1-10 nM) caused an insurmountable antagonism, thus confirming the difference in the mode of action of the two compounds. Colonic propulsion was elicited by distending a mobile rubber balloon with 0.3 ml (submaximal stimulus) or 1.0 ml (maximal stimulus) of water. The velocity of anal displacement of the balloon (mm/s) was considered the main propulsion parameter. At low concentrations (1.0-100 nM and 0.1-10 nM, respectively), MEN-10627 and SR-48968 facilitated the velocity of propulsion, whereas at high concentrations (100 nM and 1 microM, respectively) they decelerated propulsion. The excitatory and inhibitory effects of both antagonists were observed only with submaximal stimulus. We focused on the hypothesis that the facilitatory effect on propulsion may result from blockade of neuronal NK(2) receptors and the inhibitory effect from suppression of the excitatory transmission mediated by NK(2) receptors on smooth muscle cells. In the presence of N(G)-nitro-L-arginine (300 microM), a nitric oxide synthase inhibitor, MEN-10627, at a concentration (10 nM) that was found to accelerate propulsion in control experiments inhibited the velocity of propulsion. In the presence of threshold (1-10 nM) or full (1 microM) concentration of atropine, which inhibited to a great extent the velocity of propulsion, the inhibitory effect of MEN-10627 (1 microM) was markedly increased. In conclusion, in the rabbit distal colon NK(2) receptors may decelerate propulsion by activating a nitric oxide-dependent neuronal mechanism and may accelerate it by a postjunctional synergistic interaction with cholinergic muscarinic receptors.

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