Effects of Red Wine, Alcohol, and Quercetin on Coronary Resistance and Conductance Arteries

Abstract

Moderate consumption of alcoholic beverages is associated with a reduced risk of coronary heart disease (CHD). Some evidence suggests that red wine is particularly beneficial in this regard and may account in part for the French paradox, although the mechanism of this effect is unknown. We assessed the effects of red wine, ethanol, and quercetin, a major flavonoid constituent of red wine, in coronary resistance vessels (80-150 microm, i.d.) and conductance vessels (300-525 microm, i.d.) of the rabbit. Vessel wall tension was measured in isolated segments maintained in a wire-type myograph (37 degrees C) and preconstricted with 30 mM K+. At an alcohol concentration (14 mM) equivalent to moderate consumption, red wine evoked a small, transient constrictor effect in resistance and conductance vessels (9+/-4%, n = 5; 8+/-1%, n = 7, respectively; p < 0.05). Ethanol alone at this concentration was without effect. Quercetin (5.6, 8, and 30 microM) significantly relaxed resistance (-32+/-4%, n = 10; -47+/-2%, n = 7; -82+/-6%, n = 8, respectively) and conductance (-20+/-3%, n = 8; -32+/-4%, n = 8; -72+/-7%, n = 8, respectively) coronary arteries. Vasorelaxation by quercetin was endothelium-independent and was significantly greater in resistance than in conductance vessels. These data suggest that red wine and ethanol do not evoke relaxation in small coronary arteries at concentrations associated with moderate consumption. Quercetin elicits marked coronary vasorelaxation that is endothelium-independent. However, the concentrations of quercetin necessary to achieve this action are not attained with moderate red wine consumption.

Quercetin Induces Rapid eNOS Phosphorylation and Vasodilation by an Akt-Independent and PKA-Dependent Mechanism

“…The arterial vasorelaxation effect of quercetin has also been demonstrated in animal model experiments [9,10,11,12]. According to previous studies, quercetin may exert its role in both endothelium-dependent and endothelium-independent ways [13,14,15,16]. Although evidence has demonstrated that quercetin can increase eNOS activity and NO production, leading to an endothelium-dependent vasorelaxation [11,12,17], data on the molecular mechanisms of its effect are not yet entirely clear, further exploration appears worthwhile.…”

Stilbene, Ellagic Acid, Flavonol, and Phenolic Content of Muscadine Grape (Vitis rotundifolia Michx.) Cultivars

“…Quercetin, a flavonol, has been extensively studied, and has been shown to protect against DNA mutations, colon cancer and heart disease [12]. Quercetin relaxes the blood vessel wall [13] and increases the production of enzymes that dissolve blood clots [14]. Re-search has recently shown that ellagic acid combined with quercetin act together to affect the growth rate and the path by which cancer cells die.…”

On the use of food supplements

“…The -carotene data were obtained from The Alpha-Tocopherol, -Carotene Cancer Prevention Study Group, in which male smokers were daily supplemented with -carotene (20 mg). Lung cancer incidence was determined during a followup of 5-8 years [32]. Vitamin E data were obtained from Mitchel et al [50].…”

“…Arterial smooth muscles of mesenteric arteries are densely occupied with 1 -adrenoceptors. The flavonoid quercetin has previously been shown to induce vasorelaxation by reducing the sensitivity of arteries to both the 1 -adrenoceptor agonists phenylephrine and noradrenaline in arteries with and without endothelium [2,9,29,[31][32][33]. Vasorelaxation induced by the 1 -adrenoceptor blocker tamsulosin, as well of quercetin and its metabolites and combinations were determined on mesenteric arteries, to evaluate the interaction of the supplement quercetin with the drug tamsulosin.…”

“…Regarding these risks, the ATBC study revealed in 1994 that -carotene supplementation was associated with an increased incidence of lung cancer in smokers [31]. In the years that followed, other epidemiological studies corroborated this alarming effect [32][33][34][35]. The blame was put on -carotene.…”