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• W4378674313 abstract "Introduction: Excessive ethanol consume is a public health problem and it is associated with increased cardiovascular risk. We and other have previously demonstrated a key participation of renin angiotensin system (RAS) in ethanol-induced vascular abnormalities by leading to excessive reactive oxygen species (ROS) production via redox unbalance. However, whether ethanol consumption leads to vascular dysfunction by altering mitochondrial function and dynamic are unknown. We tested the hypothesis that ethanol consumption increases angiontensin II (ANG II) levels triggering mitochondria dysfunction and ROS production, which in turn promotes endothelial dysfunction. Methods: 6–8-weeks old male C57/BL6J mice were randomized in 4 groups: 1) Control; 2) Ethanol (20%, vol./vol.); 3) Losartan (10 mg/kg/feed); 4) Ethanol (20%, vol./vol.) + Losartan (10 mg/kg/feed). After 12 weeks of treatment, aortae were harvested for studies of vascular function. Results: Ethanol increased phenylephrine-induced contractility in an endothelium (Endo)-dependent manner [Maximal response (mN): Endo (+): Control: 6.1 ± 2.9, n=6; Ethanol: 11.2 ± 3.2*, n=6; Endo (-): Control: 10.8±1.4, n=5; Ethanol: 10.1±1.3, n=8). Therefore, for the next findings, we only focused on endothelium intact arteries. Remarkably, losartan treatment prevented ethanol-induced hypercontractility (Ethanol+losartan: 4.3±1.2, n=5). To study whether ethanol consumption leads to endothelial dysfunction by impairing mitochondrial function and increasing O 2 ∙- production in aorta, we used MnTMPyP (a membrane permeant Mn‐SOD mimetic, 3×10−5 M) or CCCP (a mitochondrial uncoupler, 10−6 M), respectively. Both, partially prevented the increase in contraction induced by ethanol consume. Furthermore, L-NAME (a non-specific NOS inhibitor, 10-4 M) blunted the difference between control and ethanol groups, whereas EUK 134 (a synthetic superoxide dismutase and catalase mimetic, 10-4 M) did not affect the vascular response in ethanol group, but it increased the contractility in all other groups, suggesting that nitric oxide (NO) and H2O2 bioavailability might participate of vascular dysfunctionin ethanol group. Conclusion: Our preliminary findings indicate that ethanol induces endothelial dysfunction via regulating endothelial ANGII signaling, which seems to be dependent on mitochondrial dysfunction and reduction in NO and H2O2 bioavailability. Our study may benefit the understanding of molecular and cellular mechanisms associated with ethanol consumption and cardiovascular risk and it helps advancing on treatment for cardiovascular diseases in ethanol consumers. FAPESP (2021/13075-5), NHLBI-R00 (R00HL14013903), AHA-CDA (CDA857268), Vascular Medicine Institute, the Hemophilia Center of Western Pennsylvania Vitalant, and Children's Hospital of Pittsburgh of the UPMC Health System. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process." @default.
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• W4378674313 date "2023-05-01" @default.
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• W4378674313 title "Ethanol induces endothelial dysfunction via angiotensin II: Role of mitochondrial ROS" @default.
• W4378674313 doi "https://doi.org/10.1152/physiol.2023.38.s1.5732323" @default.
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