Flavonoid-rich dark chocolate improves endothelial function and is associated with an increase in plasma epicatechin concentrations in healthy adults. No changes in oxidative stress measures, lipid profiles, blood pressure, body weight or BMI were seen.

No abstract

Losartan and captopril have similar cardiovascular protective effects in a rat model of ischemia-reperfusion. They increased the threshold of VF, decreased mortality and decreased episodes of VT and VF, as well as decreased myocardial infarct size.

1 The vasorelaxant activity of eicosapentaenoic acid (EPA,, the omega-3 polyunsaturated fatty acid, was investigated in isolated Wistar Kyoto (WKY) rat aortae by measuring isometric tension. 2 Eicosapentaenoic acid (1 ± 100 mM) relaxed rat aortae contracted with high K + (80 mM) or noradrenaline (NA, 1 mM) in a concentration-dependent manner. Contractions induced by Bay K 8644 or increasing concentrations of calcium were una ected by EPA. 3 The relaxant e ect of EPA (3 ± 100 mM) was signi®cantly inhibited by indomethacin (10 mM), the cyclo-oxygenase inhibitor, but not by the nitric oxide (NO) synthesis inhibitor, N o -nitro-L-arginine methyl ester hydrochloride (L-NAME, 100 mM). Removal of the endothelium did not alter EPAinduced relaxations. 4 In Ca 2+ -free, EGTA 2 mM solution, EPA (10 ± 30 mM signi®cantly inhibited NA-sustained contractions. Incubation with EPA (5, 10 mM) diminished both NA-induced (1 mM) phasic and sustained contractions. 5 The vasorelaxant e ects of EPA (530 mM) on NA-induced (1 mM) contractions were signi®cantly inhibited by the K + channel blocker, glibenclamide (10 mM), but not tetraethylammonium (1 mM). Moreover, indomethacin and glibenclamide combined signi®cantly inhibited EPA-induced (1 ± 100 mM) responses. 6 These results indicate EPA exerts its endothelium-independent vasorelaxant e ects in WKY rat aortae through production of prostanoids which activate K + ATP channels. Inhibition of Ca 2+ mobilization from intracellular pools and in¯ux through the non-L-type, but not the L-type, Ca 2+ channel are also possible mechanisms action of EPA's.

Captopril, quinapril, and losartan had similar protective effects against atherogenesis. Captopril and quinapril were more effective than losartan in preserving vascular function. Increased bradykinin by ACE inhibition may be responsible for this improved vascular endothelial function.