Resveratrol, a phenolic substance present in grapes and a variety of medical plants, has been reported to induce vasorelaxation, however the mechanisms are uncertain. In this paper we investigate the possible participation of K π channels in the endothelium-independent vasodilatation of rat aorta induced by resveratrol. Resveratrol induced concentration-dependent relaxation of rings with endothelium and without endothelium. We used different potassium channel inhibitors to determine whether the K π channels mediated endothelium-independent relaxation of rat aorta induced by resveratrol. Highly selective blocker of ATP-sensitive K π channels, glibenclamide, as well as non-selective blockers of K π channels, tetraethylammonium, did not block resveratrol-induced relaxation of rat aortic rings. Charybdotoxin, a blocker of calcium-sensitive K π channels did not affect the resveratrol-induced relaxation. 4-Aminopiridine, non-selective blocker of voltage-gated K π (Kv) channels, and margatoxin that inhibits Kv1 channels abolished relaxation of rat aortic rings induced by resveratrol. In conclusion, we have shown that resveratrol potently relaxed rat aortic rings with denuded endothelium. It seems that 4-aminopiridine and margatoxin-sensitive K π channels located in the smooth muscle of rat aorta mediated this relaxation.

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To evaluate phasic function and deformation of the left atrium (LA) and right atrium (RA) in subjects with prediabetes and type 2 diabetes mellitus. This cross-sectional study included 50 untreated normotensive subjects with prediabetes, 60 recently diagnosed normotensive diabetic patients and 60 healthy controls of similar sex and age. All the subjects underwent laboratory analyses and complete echocardiographic examination including strain analysis. LA and RA reservoir and conduit function gradually decreased, while booster pump increased, from the healthy controls, throughout the prediabetics, to the diabetics. The strain analysis of atrial phasic function showed more regular pattern of progressive atrial function deterioration than conventional evaluation with total, active and passive atrial function. In the whole study population HbA1c correlated with LA passive emptying fraction (r = -0.38, p < 0.01), LA active emptying fraction (r = 0.36, p < 0.01), LA longitudinal strain during systole (r = -0.35, p < 0.01), RA passive emptying fraction (r = -0.42, p < 0.01), RA active emptying fraction (r = 0.38, p < 0.01), and RA longitudinal strain during systole (r = -0.32, p < 0.01). However, only LA passive emptying fraction (β = -0.32, p < 0.01) and LA longitudinal strain during systole (β = -0.28, p = 0.02) were independently associated with HbA1c among the LA parameters; whereas solely RA passive emptying fraction (β = -0.37, p < 0.01) and RA active emptying fraction (β = 0.31, p = 0.01) were independently associated with HbA1c among the RA parameters. LA and RA phasic functions are significantly impaired in the prediabetics and the diabetics. The parameter of glucose control correlated with LA and RA reservoir, conduit and pump atrial function.

Left ventricular deformation obtained by 3DE is significantly impaired in the type 2 DM patients. HbA1c is independently associated with LV mechanics that implies that early anti-diabetic therapy and normalization of the fasting glucose level and HbA1c could impede further cardiac damage.

The blood flow from the placenta to the fetus depends on human umbilical vein (HUV) vascular tone. ATP-sensitive K(+) (K(ATP)) channels link the metabolic state of the cell to membrane potential, and their activation in the HUV represents protection against hypoxia. The aims of our study were to assess the effects of resveratrol and naringenin on the HUV and to define the roles of K(ATP) channels in their effects. Serotonin or 100 mM K(+) were used for precontraction of the HUV without endothelium. The cumulative concentration-response curves were obtained by adding increasing concentrations of resveratrol or naringenin. Glibenclamide was used, in order to test the role of K(ATP) channels in its effect. Resveratrol induced more potent vasodilatation of serotonin- and 100 mM K(+)-precontracted HUV than naringenin. Glibenclamide induced significant shift to the right of the concentration-response curves of resveratrol and P1075 (a specific opener of K(ATP) channels). Western blotting showed that HUV expressed protein Kir6.1. Thus, resveratrol and naringenin produce dilatation of HUV. It seems that K(ATP) channels are involved in the relaxation of HUV induced by resveratrol, while naringenin seems to interact with other ion channels. The K(+) channel-independent mechanism(s) of these polyphenols could not be excluded.