Ethanol withdrawal increases oxidative stress and reduces nitric oxide bioavailability in the vasculature of rats

Gonzaga, Natália A.; Mecawi, André Souza; Antunes‐Rodrigues, José; Martinis, Bruno Spinosa De; Padovan, Cláudia Maria; Tirapelli, Carlos Renato

doi:10.1016/j.alcohol.2014.12.001

Cited by 36 publications

(23 citation statements)

References 32 publications

(49 reference statements)

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“…Indeed, the systolic and mean arterial pressures in W rats, although lower than in ET rats, were still significantly higher than in controls. Little is known about the effects of withdrawal on BP and the few existing studies have focused on the effects of acute withdrawal [19, 20]. It was previously shown that BP increases after acute ethanol abstinence both in humans [19] and in rats consuming low doses of ethanol for 20 days [20].…”

Section: Discussionmentioning

confidence: 99%

“…It was previously shown that BP increases after acute ethanol abstinence both in humans [19] and in rats consuming low doses of ethanol for 20 days [20]. Despite the differences between our animal model of ethanol consumption and those from Gonzaga and collaborators [20], which was longer and with a higher amount of ethanol consumed (24 weeks of 20% v/v versus 21 days of 3-9% v/v), we extended their results by showing that the increase in BP persists even after long-term withdrawal. This is a relevant finding since it provides evidence for an increased risk for later onset of cardiovascular diseases [19].…”

Section: Discussionmentioning

confidence: 99%

“…Little is known about the effects of withdrawal on BP and the few existing studies have focused on the effects of acute withdrawal [19, 20]. It was previously shown that BP increases after acute ethanol abstinence both in humans [19] and in rats consuming low doses of ethanol for 20 days [20]. Despite the differences between our animal model of ethanol consumption and those from Gonzaga and collaborators [20], which was longer and with a higher amount of ethanol consumed (24 weeks of 20% v/v versus 21 days of 3-9% v/v), we extended their results by showing that the increase in BP persists even after long-term withdrawal.…”

Section: Discussionmentioning

confidence: 99%

“…Although it is widely known that heavy ethanol consumption has hypertensive effects [4-13] and can induce impairment of several organs [6, 10-16], its effects on kidney structure and function remain to be elucidated [16-18]. Moreover, very few clinical and experimental studies evaluated BP alterations underlying alcohol withdrawal and particularly after acute withdrawal [19, 20], but there are no follow up studies in the absence of alcohol consumption, specifically its consequences on BP and kidney structure.…”

Section: Introductionmentioning

confidence: 99%

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Heavy Alcohol Consumption Effects on Blood Pressure and on Kidney Structure Persist After Long-Term Withdrawal

Leal

Jorge

Barbosa

et al. 2017

Kidney Blood Press Res

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Background/Aims: Heavy ethanol consumption is a risk factor for hypertension and prompts organ damage. There is no information regarding the impact of long-term heavy ethanol consumption on kidney structure and function linking to their hypertensive effects nor the repercussions after withdrawal. Methods: Rats were exposed to ethanol for 24 weeks and, afterwards, a group was assigned to withdrawal for 8 weeks. Blood pressure (BP) was measured and serum biochemical parameters were quantified. Glomerular volume density, areal density of glomerular tuft and renal corpuscles were determined. Angiotensin II type 1 receptor (AT1R) protein expression was evaluated. Results: Twenty-four weeks of ethanol consumption causes atrophy of renal corpuscles and glomeruli and reduces the volume of glomeruli. Glomerular changes induced by ethanol consumption were still evident after withdrawal. Renal AT1R levels were increased in ethanol-treated rats and returned to control levels during withdrawal. Ethanol consumption also induced an increase in BP, uric acid and albumin levels. Upon withdrawal, systolic and mean arterial pressures decreased, but were still higher than in controls rats. Conclusion: Ethanol consumption induces changes in glomerular morphology associated with increased BP and AT1R expression. Long-term withdrawal was inefficient to restore the structural integrity of renal corpuscles and in lowering systolic pressure.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Heavy Alcohol Consumption Effects on Blood Pressure and on Kidney Structure Persist After Long-Term Withdrawal

Leal

Jorge

Barbosa

et al. 2017

Kidney Blood Press Res

View full text Add to dashboard Cite

show abstract

“…(11), (12), (13) Meanwhile, some recent studies have shown increased oxidative stress during the alcohol withdrawal state also. (14), (15), (16) As this was found to correlate with glutamatergic excitotoxicity of the withdrawal state, it was put forth as a possible mechanism mediating the symptoms of alcohol withdrawal. (17) The oxidative stress parameters showed correlation with the severity of withdrawal state.…”

Section: Introductionmentioning

confidence: 99%

Higher Oxidative Stress in Current Alcoholics Compared to Abstinent Alcoholics and Normal Controls: A Cross-Sectional Study

Sandhya¹,

Sreekumari²,

Vidhukumar³

2016

jemds

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Reactive oxygen species derived from NAD(P)H oxidase play a role on ethanol-induced hypertension and endothelial dysfunction in rat resistance arteries

et al. 2016

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Chronic ethanol consumption is a risk factor for cardiovascular diseases. We studied whether NAD(P)H oxidase-derived reactive oxygen species (ROS) play a role in ethanol-induced hypertension, vascular dysfunction, and protein expression in resistance arteries. Male Wistar rats were treated with ethanol (20 % v/v) for 6 weeks. Ethanol treatment increased blood pressure and decreased acetylcholine-induced relaxation in the rat mesenteric arterial bed (MAB). These responses were attenuated by apocynin (30 mg/kg/day; p.o. gavage). Ethanol consumption increased superoxide anion (O) generation and decreased nitrate/nitrite (NO ) concentration in the rat MAB and apocynin prevented these responses. Conversely, ethanol did not affect the concentration of hydrogen peroxide (HO) and reduced glutathione (GSH) or the activity of superoxide dismutase (SOD) and catalase (CAT) in the rat MAB. Ethanol increased interleukin (IL)-10 levels in the rat MAB but did not affect the levels of tumor necrosis factor (TNF)-α, IL-6, or IL-1β. Ethanol increased the expression of Nox2 and the phosphorylation of SAPK/JNK, but reduced eNOS expression in the rat MAB. Apocynin prevented these responses. However, ethanol treatment did not affect the expression of Nox1, Nox4, p38MAPK, ERK1/2, or SAPK/JNK in the rat MAB. Ethanol increased plasma levels of TBARS, TNF-α, IL-6, IL-1β, and IL-10, whereas it decreased NO levels. The major finding of our study is that NAD(P)H oxidase-derived ROS play a role on ethanol-induced hypertension and endothelial dysfunction in resistance arteries. Moreover, ethanol consumption affects the expression and phosphorylation of proteins that regulate vascular function and NAD(P)H oxidase-derived ROS play a role in such responses.

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Ethanol withdrawal increases oxidative stress and reduces nitric oxide bioavailability in the vasculature of rats

Cited by 36 publications

References 32 publications

Heavy Alcohol Consumption Effects on Blood Pressure and on Kidney Structure Persist After Long-Term Withdrawal

Heavy Alcohol Consumption Effects on Blood Pressure and on Kidney Structure Persist After Long-Term Withdrawal

Higher Oxidative Stress in Current Alcoholics Compared to Abstinent Alcoholics and Normal Controls: A Cross-Sectional Study

Reactive oxygen species derived from NAD(P)H oxidase play a role on ethanol-induced hypertension and endothelial dysfunction in rat resistance arteries

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