2017
DOI: 10.1016/j.jff.2017.04.035
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The red wine polyphenol, resveratrol improves hemodynamics, oxidative defence and aortal structure in essential and malignant hypertension

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Cited by 17 publications
(19 citation statements)
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“…It is well known that arterial hypertension is associated with a rise in reactive oxygen species (ROS) [ 49 , 50 ]. Several studies have shown alteration of oxidative status in LNHR and an improvement after treatment with an antioxidant substance [ 51 , 52 ].…”
Section: Discussionmentioning
confidence: 99%
“…It is well known that arterial hypertension is associated with a rise in reactive oxygen species (ROS) [ 49 , 50 ]. Several studies have shown alteration of oxidative status in LNHR and an improvement after treatment with an antioxidant substance [ 51 , 52 ].…”
Section: Discussionmentioning
confidence: 99%
“…Malignant hypertension can develop from essential hypertension through serious long-term inhibition of endothelium-derived, vasodilatory, nitric oxide (NO). In particular, persistent N G -L-Arginine Methyl Ester (L-NAME) ( Figure 1 B) inhibition of NO biosynthesis in SHRs leads to a significant increase in blood pressure followed by profound vasoconstriction, oxidative stress, and structural alterations of the conduit and large arteries, as well as cardiac hypertrophy [ 4 , 5 , 6 ].…”
Section: Introductionmentioning
confidence: 99%
“…It is found in all cell types of the cardiovascular system, including cardiac myocytes, vascular smooth muscle, endothelial cells, fibroblasts, and blood cells [ 15 ]. The endothelial cell dysfunction in hypertension relates to the abundance of TGF-β in the arterial wall, which promotes intimal proliferation as well as the development of vascular lesions accompanied by apoptosis in the vascular smooth muscle cells [ 5 ].…”
Section: Introductionmentioning
confidence: 99%
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“…The mechanism of RSV on blood vessels mainly was explained through its effects on endothelium. Endothelium-dependent mechanisms of relaxation by RSV include stimulation of endothelial NO production, inhibition of superoxide-mediated NO inactivation (1,15) and stimulation of endothelium dependent hyperpolarization (EDH) (16). The endothelium-independent relaxation is partly mediated by different K channels in the membrane of vascular smooth muscle cells, including voltage-gated K (Kv) channels, big Ca-activated K (BK Ca ) channels, but not adenosine triphosphate-sensitive K (K ATP ) channels (5,6).…”
Section: Introductionmentioning
confidence: 99%