EFFECTS OF CHRONIC ETHANOL CONSUMPTION ON Α-Adrenergic-Induced CONTRACTIONS AND ENDOTHELIUM-DEPENDENT RELAXATIONS IN RAT THORACIC AORTA

Şahna, Engin; Kurçer, Zehra; Öztürk, Feral; Cengiz, Nurettin; Vardı, Nigar; Birincioğlu, Mustafa; Ölmez, Ercüment

doi:10.1006/phrs.1999.0629

Cited by 15 publications

(11 citation statements)

References 22 publications

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“…On the other hand, unchanged (Chan and Sutter, 1983;Utkan et al, 2001) or attenuated (Strickland and Wooles, 1988) responses to ␣ 1 -adrenoceptor agonists have also been described. Reasons for these differences are not clear, although it was suggested that they could be explained by different experimental conditions, including the type of artery or agonist examined, the method used for vascular studies, different concentration of ethanol used, different experimental model, or the duration of chronic ethanol treatment (Pinardi et al, 1992;Sahna et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…The reason for these differences is not entirely clear, but contributing factors may be different experimental designs, different protocols of ethanol administration, or the duration of chronic treatment. The periods of chronic ethanol treatment differ among the several studies published (from 18 days to 24 weeks) (Pinardi et al, 1992;Sahna et al, 2000). Moreover, the majority of the experiments designed to study the vascular effects of chronic ethanol consumption on ␣ 1 -induced contraction use only one period of treatment (Chan and Sutter, 1983;Utkan et al, 2001;Brown et al, 2002).…”

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Chronic Ethanol Consumption Enhances Phenylephrine-Induced Contraction in the Isolated Rat Aorta

Tirapelli¹,

Al-Khoury²,

Bkaily³

et al. 2005

J Pharmacol Exp Ther

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Changes in reactivity to phenylephrine in aortas isolated from 2-, 6-, and 10-week ethanol-treated rats and their age-matched control and isocaloric rats were investigated. Chronic ethanol consumption enhances the contractile response of endothelium-intact and -denuded rat aortic rings to phenylephrine, a response that is time-independent. Pretreatment with indomethacin reduced E max for phenylephrine in denuded aortas from ethanol-treated rats but not control or isocaloric rats. After indomethacin treatment, no differences in E max from phenylephrine were observed among the groups.-5-heptenoic acid), an antagonist of prostaglandin H 2 /thromboxane A 2 (TXA 2 ) receptors, did not alter phenylephrine-induced contraction in control or isocaloric aortas. However, in ethanol-treated aortas, E max was reduced to control level. Moreover, phenylephrine-stimulated release of thromboxane B 2 , a stable metabolite of TXA 2 , was higher in tissues from ethanol-treated rats. Simultaneous measurement of the changes in [Ca 2ϩ ] i and contraction induced by phenylephrine showed that both parameters are higher in the rat aorta from ethanol-treated rats. CaCl 2 -induced contraction in free Ca 2ϩ solution containing phenylephrine was increased in ethanol-treated aortas. Additionally, the enhancement in CaCl 2 -induced contraction was prevented by SQ29548. The major contribution of the present study is that it demonstrates a detailed description of the mechanisms involved in the enhancement of phenylephrine-induced contraction in rat aorta from ethanol-treated rats. We provided evidence that this response was not different among the three periods of treatment employed in this study and that it is maintained by two mechanisms: an increased release of vascular smooth musclederived vasoconstrictor prostanoids (probably TXA 2 ) and an enhanced extracellular Ca 2ϩ influx.Chronic ethanol consumption is associated with cardiovascular dysfunctions independent of other known risk factors (Altura and Altura, 1982). Much of the research investigating the chronic effects of ethanol on the cardiovascular system has dealt with vascular responsiveness to vasoconstrictor agents (Strickland and Wooles, 1988;Hatton et al., 1992). Previous reports suggest that enhanced vascular reactivity to vasoconstrictor agents (Pinardi et al., 1992) or impairment of the vascular relaxation (Kahonen et al., 1999) contribute to the cardiovascular complications associated with chronic ethanol consumption.Enhanced vascular reactivity to ␣ 1 -adrenoceptor agonists was demonstrated in different arteries from ethanol-treated rats. In this line, Pinardi et al. (1992) found that chronic ethanol consumption significantly enhanced the contractile response induced by phenylephrine in aortic rings with intact endothelium. The contractile response of superior mesenteric artery to noradrenaline was shown to be greater in the rings from ethanol-treated rats (Hatton et al., 1992). Likewise, Stewart and Kennedy (1999) demonstrated an ethanol-associated increase in the m...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Chronic Ethanol Consumption Enhances Phenylephrine-Induced Contraction in the Isolated Rat Aorta

Tirapelli¹,

Al-Khoury²,

Bkaily³

et al. 2005

J Pharmacol Exp Ther

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“…Studies that have applied the developmental origins of health and disease approach reveal that adult‐onset diseases (cardiovascular, diabetes, obesity, and cognitive decline) appear to be programmed in utero in response to maternal exposure to many types of stimuli. Support for this concept can be found in studies suggesting that in utero exposure to a variety of agents and environmental stimuli can contribute to diseases in adulthood by targeting the endothelium and vascular function (Care et al., ; Gray et al., ; Jones et al., ; Sahna et al., ), suggesting mechanistic effects beyond toxicity‐induced cell death. With regard to in utero exposure to alcohol, studies have shown a significant increase in cardiovascular abnormalities (atrial septal defects, ventricular septal defects, and other malformations in blood vessels) in infants and children with FASD (Davidson, ; Jones et al., ; Löser and Majewski, ).…”

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confidence: 99%

In Utero Exposure to Alcohol Impairs Reactivity of Cerebral Arterioles and Increases Susceptibility of the Brain to Damage Following Ischemia/Reperfusion in Adulthood

Cananzi

Mayhan

2019

Alcoholism Clin & Exp Res

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Background: Maternal consumption of alcohol produces abnormalities in the developing fetus and can contribute to an increased incidence of many cardiovascular-related diseases. The first goal of this study was to determine whether in utero exposure to alcohol influences reactivity of cerebral arterioles in adult (12 to 15 weeks old) rats. The second goal of this study was to examine whether in utero exposure to alcohol increased the susceptibility of the brain to damage following an ischemic event in adult rats.Methods: We fed Sprague Dawley dams a liquid diet with or without alcohol (3% ethanol) for the duration of their pregnancy (21 to 23 days). In the first series of studies, we examined reactivity of cerebral arterioles to endothelial nitric oxide synthase (eNOS)-(adenosine diphosphate [ADP]) and neuronal nitric oxide synthase (nNOS)-dependent N-methyl-D-aspartate (NMDA, and NOS-independent agonists in adult rats before and during application of L-NMMA. In another series of studies, we examined infarct volume following middle cerebral artery occlusion in adult offspring exposed to alcohol in utero. In both series of studies, we also determined the role for an increase in oxidative stress by feeding dams apocynin for the duration of their pregnancy.Results: We found that in utero exposure to alcohol reduced responses of cerebral arterioles to ADP and NMDA, but not to nitroglycerin in adult rats. In addition, treatment of the dams with apocynin prevented this impairment in cerebral vascular function. We also found that in utero exposure to alcohol worsened brain damage following ischemia/reperfusion in adult rats and that treatment of dams with apocynin prevented this increase in brain damage following ischemia/reperfusion.Conclusions: We suggest that our findings may have important implications for the pathogenesis of brain abnormalities associated with fetal alcohol exposure.

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“…However, some reports suggest that chronic ethanol consumption may cause enhanced or attenuated contractions of rat aorta to PE [13,14]. Reasons for these differences are not clear, although it has been suggested that they could be explained by different experimental conditions, including the duration of chronic ethanol treatment or the method used for the studies [15,16].…”

Section: Discussionmentioning

confidence: 99%

Chronic alcoholism associated with diabetes impairs erectile function in rats

Lizarte¹,

Morgueti²,

Tirapelli³

et al. 2010

BJU International

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Immunoexpression of endothelial NO synthase (eNOS) and inducible NOS (iNOS) was also accessed. RESULTSThe endothelium-dependent relaxation induced by ACh was decreased in CSM from ethanol-diabetic rats when compared with the controls, with a mean ( SEM ) of 21 (4) vs 37 (2)%. Similarly, the potency and maximal responses induced by SNP were reduced in the ethanol-diabetic [3.97 (0.38) and 85 (1)%, respectively] and diabetic groups [3.78 (0.56) and 81 (2)%, respectively] when compared with the controls [5.3 (0.22) and 90 (3)%, respectively] and isocaloric [5.3 (0.19) and 92 (1)%, respectively] groups. Noradrenergic nerve-mediated contractions of CSM in response to EFS were increased in rats from ethanol-diabetic and diabetic groups when compared with the control and isocaloric groups. Conversely, there were no differences in EFS-induced relaxation among the groups. The immunostaining assays showed overexpression of eNOS and iNOS in the CSM from diabetic and ethanol-diabetic rats when compared with the control and isocaloric rats. CONCLUSIONThere was an impairment of relaxation of CSM from ethanol-diabetic and diabetic rats that involved a decrease in the NO-cyclic guanosine monophosphate signalling pathway by endothelium-dependent mechanisms accompanied by a change in the CSM contractile sensitivity.

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EFFECTS OF CHRONIC ETHANOL CONSUMPTION ON Α-Adrenergic-Induced CONTRACTIONS AND ENDOTHELIUM-DEPENDENT RELAXATIONS IN RAT THORACIC AORTA

Cited by 15 publications

References 22 publications

Chronic Ethanol Consumption Enhances Phenylephrine-Induced Contraction in the Isolated Rat Aorta

Chronic Ethanol Consumption Enhances Phenylephrine-Induced Contraction in the Isolated Rat Aorta

In Utero Exposure to Alcohol Impairs Reactivity of Cerebral Arterioles and Increases Susceptibility of the Brain to Damage Following Ischemia/Reperfusion in Adulthood

Chronic alcoholism associated with diabetes impairs erectile function in rats

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