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  • Vinegar intake enhances flow-mediated vasodilatation via upregulation of endothelial nitric oxide synthase activity.

Vinegar intake enhances flow-mediated vasodilatation via upregulation of endothelial nitric oxide synthase activity.

Bioscience, biotechnology, and biochemistry (2010-05-13)
Syoji Sakakibara, Ryuichiro Murakami, Mikio Takahashi, Takashi Fushimi, Toyoaki Murohara, Mikiya Kishi, Yoshitaka Kajimoto, Masafumi Kitakaze, Takayuki Kaga
ZUSAMMENFASSUNG

This study examined the effect of acetate on endothelial nitric oxide synthase (eNOS) in human umbilical vein endothelial cells (HUVECs) by immunoblotting assay and the ability of acetic acid to upregulate flow-mediated vasodilatation in humans. In HUVECs, acetate induced a biphasic increase in the phosphorylated form of eNOS. The amount of phosphorylated eNOS was significantly increased by exposure to 200 mumol/l acetate for 20 min (early phase) and for 4 h (late phase). The inhibitors of cAMP-dependent protein kinase (PKA) and AMP-activated protein kinase (AMPK) blocked acetate-induced eNOS phosphorylation in the early and the late phase respectively. Furthermore, in postmenopausal women, maximum forearm blood flow (FBF) in response to shear stress increased in the vinegar (acetic acid) administered group compared to the placebo group. These results suggest that acetic acid-induced eNOS phosphorylation contributes to upregulation of flow-mediated vasodilatation in humans.

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AMPK-Inhibitor, Verbindung C, AMPK Inhibitor, Compound C, CAS 866405-64-3, is a cell-permeable compound that inhibits KDR/VEGFR2, ALK2/BMPR-I, and AMPK kinase activities (IC50 = 25.1, 148, and 234.6 nM, respectively).
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8-Cyclopentyl-1,3-dipropylxanthine, solid
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8-(3-Chlorostyryl)caffeine, ≥98% (HPLC), solid
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MRS 1754 hydrate, ≥98% (HPLC), solid