Beneficial vs. detrimental actions of ethanol on heart and coronary vascular muscle: Roles of Mg2+ and Ca2+

Altura, Burton M.; Zou, Li; Altura, Bella T.; Jelicks, Linda A.; Wittenberg, Beatrice A.; Gupta, Raj K.

doi:10.1016/0741-8329(96)00044-4

Cited by 22 publications

(9 citation statements)

References 66 publications

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“…In general, it has been reported that higher doses of alcohol depress cardiac function and cardiac myocyte contractility and metabolism [5,24,25]. This appears to be a consistent finding both in vivo and in vitro.…”

Section: Discussionsupporting

confidence: 65%

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Ethanol Reduces Cardiac Myocyte Function through Activation of the Nitric Oxide-Cyclic GMP Pathway

Weiss¹,

Haïm

Zhang

et al. 2003

Pharmacology

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We tested the hypothesis that low-dose ethanol would reduce cardiac myocyte function through increased production in the nitric oxide/cyclic GMP signal transduction pathway, rather than reduced degradation. Ventricular myocytes were isolated from the hearts of 9 rabbits. Myocyte function was studied using a video-edge detector and cyclic GMP levels were measured by radioimmunoassay. Cells were administered 5 and 10 mmol/l ethanol alone or after 10^–6 mol/l N^G-nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhibitor), 10^–6 mol/l 1H-[1,2,4]oxadiazolo[4,3a]quinoxalin-1-one (ODQ, soluble guanylyl cyclase inhibitor) or 10^–5 mol/l zaprinast (cyclic GMP phosphodiesterase inhibitor). Ethanol (10 mmol/l) significantly decreased percent shortening from 10.0 ± 0.9 to 6.0 ± 0.2%. Similar decrements occurred in the maximum rate of shortening and relaxation. After L-NAME or ODQ, the decrements in percent shortening, maximum rate of shortening and relaxation caused by ethanol were not significant. After zaprinast, ethanol significantly decreased the maximum rate of shortening and relaxation and percent shortening to 4.3 ± 0.5. Ethanol (10 mmol/l) significantly increased cyclic GMP from 403 ± 121 to 529 ± 128 fmol/10⁵ myocytes. Both L-NAME and ODQ lowered cyclic GMP, and ethanol did not affect cyclic GMP after either. Zaprinast raised cyclic GMP, as did its combination with 10 mmol/l ethanol (653 ± 120). Thus, ethanol both reduced myocyte function and increased cyclic GMP. Blocking nitric oxide production or guanylyl cyclase activity prevent these effects of ethanol, while blocking cyclic GMP degradation did not. This suggests that ethanol acts as a nitric oxide stimulator in ventricular myocytes leading to reduced function and increased cyclic GMP.

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Section: Discussionsupporting

confidence: 65%

“…This appears to be a consistent finding both in vivo and in vitro. With low to moderate doses of ethanol both increases and decreases in cardiac function and metabolism have been reported [6,11,25,25]. It is difficult to separate the direct from the reflex effects of alcohol.…”

Section: Discussionmentioning

confidence: 99%

Ethanol Reduces Cardiac Myocyte Function through Activation of the Nitric Oxide-Cyclic GMP Pathway

Weiss¹,

Haïm

Zhang

et al. 2003

Pharmacology

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“…Changes in NO levels may partly explain the variable dilatory and constrictive effects reported for alcohol in different vascular beds [54,55,56,57]. Other mechanisms likely include ethanol-induced changes in the levels of the vasodilator prostacyclin (PGI 2 ) [58] or the potent vasoconstrictor endothelin-1 [59], as well as changes in intracellular Ca 2+ [54,60,61] and Mg 2+ levels [62]. With respect to vasoreactivity and alcohol, once again there is evidence of opposite effects of low-moderate (vasodilatory) vs .…”

Section: Alcohol and Nitric Oxide (No)mentioning

confidence: 99%

Alcohol and Cardiovascular Disease—Modulation of Vascular Cell Function

Cahill

Redmond

2012

Nutrients

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Alcohol is a commonly used drug worldwide. Epidemiological studies have identified alcohol consumption as a factor that may either positively or negatively influence many diseases including cardiovascular disease, certain cancers and dementia. Often there seems to be a differential effect of various drinking patterns, with frequent moderate consumption of alcohol being salutary and binge drinking or chronic abuse being deleterious to one’s health. A better understanding of the cellular and molecular mechanisms mediating the many effects of alcohol consumption is beginning to emerge, as well as a clearer picture as to whether these effects are due to the direct actions of alcohol itself, or caused in part by its metabolites, e.g., acetaldehyde, or by incidental components present in the alcoholic beverage (e.g., polyphenols in red wine). This review will discuss evidence to date as to how alcohol (ethanol) might affect atherosclerosis that underlies cardiovascular and cerebrovascular disease, and the putative mechanisms involved, focusing on vascular endothelial and smooth muscle cell effects.

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“…The contractile cardiomyocytes are greatly affected by high doses of ethanol (EtOH) (100 to 200 mM) leading to apoptosis and later necrosis (>24 hours) (Altura et al, 1996; Doser et al, 2009; Guan et al, 2004; Kandadi et al, 2013). Apoptotic changes are mainly orchestrated through caspase 3 (Porter and Janicke, 1999).…”

mentioning

confidence: 99%

Acute Alcohol Modulates Cardiac Function as PI3K/Akt Regulates Oxidative Stress

Umoh

Walker

AlRubaiee

et al. 2014

Alcohol Clin Exp Res

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Background Clinical manifestations of alcohol abuse on the cardiac muscle include defective contractility with the development of heart failure. Interestingly, low alcohol consumption has been associated with reduced risk of cardiovascular disease. Although several hypotheses have been postulated for alcoholic cardiomyopathy and for the low-dose beneficial cardiovascular effects, the precise mechanisms and mediators remain largely undefined. We hypothesize that modulation of oxidative stress by PI3K/Akt plays a key role in the cardiac functional outcome to acute alcohol exposure. Methods Thus, acutely exposed rat cardiac tissue and cardiocytes to low (LA: 5 mM), moderate (MA: 25 mM), and high (HA: 100 mM) alcohol were assessed for markers of oxidative stress in the presence and absence of PI3K/Akt activators (IGF-1 0.1 μM or constitutively active PI3K: Ad.BD110 transfection) or inhibitor (LY294002 1 μMor Akt-negative construct Ad.Akt(K179M) transfection). Results Acute LA reduced Akt, superoxide dismutase (SOD-3) and NFκB, ERK1, and p38 MAPK gene expression. Acute HA only increased that of SOD-3 and NFκB. These effects were generally inhibited by Ad.Akt(K179M) and enhanced with Ad.BD110 transfection. In parallel, LA reduced but HA enhanced Akt activity, which was reversed by IGF-1 and inhibited by Ad.Akt(K179M), respectively. Also, LA reduced caspase 3/7 activity and oxidative stress, while HA increased both. The former was blocked, while the latter effect was enhanced by Ad.Akt(K179M). The reverse was true with PI3K/Akt activation. This translated into reduced viability with HA, with no effect with LA. On the functional level, acute LA improved cardiac output and ejection fraction, mainly through increased stroke volume. This was accompanied with enhanced end-systolic pressure–volume relationship and preload recruitable stroke work. Opposite effect was recorded for HA. LA and HA in vivo functional effects were alleviated by LY and enhanced by IGF-1 treatment. Conclusions Acute LA and HA seem to oppositely affect cardiac function through modulation of oxidative stress where PI3K/Akt plays a pivotal role.

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Beneficial vs. detrimental actions of ethanol on heart and coronary vascular muscle: Roles of Mg2+ and Ca2+

Cited by 22 publications

References 66 publications

Ethanol Reduces Cardiac Myocyte Function through Activation of the Nitric Oxide-Cyclic GMP Pathway

Ethanol Reduces Cardiac Myocyte Function through Activation of the Nitric Oxide-Cyclic GMP Pathway

Alcohol and Cardiovascular Disease—Modulation of Vascular Cell Function

Acute Alcohol Modulates Cardiac Function as PI3K/Akt Regulates Oxidative Stress

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