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  • 1.
    Díaz, Miguel
    et al.
    The Swedish Red Cross University College, Department of Health Sciences. Manchester Metropolitan University, Manchester, UK.
    Parikh, Vijay
    Manchester Metropolitan University, Manchester, UK.
    Ismail, Saira
    Manchester Metropolitan University, Manchester, UK.
    Maxamed, Raja
    Manchester Metropolitan University, Manchester, UK.
    Tye, Emily
    Manchester Metropolitan University, Manchester, UK.
    Austin, Clare
    Edge Hill University, Lancashire, UK.
    Dew, Tristan
    Manchester Metropolitan University, Manchester, UK.
    Graf, Brigitte A
    Manchester Metropolitan University, Manchester, UK.
    Vanhees, Luc
    University Leuven, Leuven, Belgium.
    Degens, Hans
    Manchester Metropolitan University, Manchester, UK / Lithuanian Sports University, Kaunas, Lithuania / University of Medicine and Pharmacy of Targu Mures, Romania..
    Azzawi, May
    Manchester Metropolitan University, Manchester, UK.
    Differential effects of resveratrol on the dilator responses of femoral arteries, ex vivo2019In: Nitric oxide, ISSN 1089-8603, E-ISSN 1089-8611, Vol. 92, p. 1-10Article in journal (Refereed)
    Abstract [en]

    Resveratrol is a plant-derived phytoalexin with antioxidant, anti-inflammatory and cardio-protective properties and may be a promising therapeutic intervention strategy in cardiovascular disease. Here, we investigated the acute direct effects of trans-resveratrol (RV), on acetylcholine (ACh)-induced and flow-mediated dilation (FMD) of isolated pressurized femoral arteries of young (4-month-old) and old (26-month-old) mice. Vessel exposure to RV enhanced ACh (0.01-1.0 mM)-induced dilation (p < 0.05), but not FMD (@ 5-10 μL⋅min-1) (p < 0.05) in both young and old mice. After RV incubation, acute nitric oxide (NO) production by cultured endothelial cells was increased in response to 0.01 mM ACh, but reduced by flow (5-10 μL⋅min-1; p < 0.05). In isolated femoral arteries from endothelial nitric oxide synthase knockout (eNOS-/-) mice, RV had no overall effect on flow mediated dilation, but potentiated ACh induced dilation, that was completely abolished by potassium channel blockers, Apamin and Tram 34 (p < 0.01). We demonstrate that the non-metabolised form of RV stimulates ACh-induced dilation via the NO and EDHF pathways, but not FMD by interaction with the cyclo-oxygenase pathway. Our findings have important implications in the use of RV (for both young and aged) under 'normal' non-diseased physiological states.

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