Effects of chronic ethanol consumption on α-adrenergic-induced contractions in rat thoracic aorta

Pinardi, G.; Brieva, Claudia; Vinet, Raúl; Penna, Mario

doi:10.1016/0306-3623(92)90019-g

Cited by 40 publications

(30 citation statements)

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“…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).…”

mentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

“…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.…”

mentioning

confidence: 99%

“…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.…”

mentioning

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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confidence: 99%

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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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mentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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

Şahna¹,

Kurçer²,

Öztürk

et al. 2000

Pharmacological Research

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Physiological basis for effect of physical conditioning on chronic ethanol-induced hypertension in a rat model

2006

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The study aim was to investigate the interaction of physical conditioning and chronic ethanol ingestion on blood pressure (BP), heart rate (HR), nitric oxide (NO) and oxidants/antioxidants balance in the plasma of rats. Male Fisher rats were divided into four groups of seven animals each and treated as follows: (1) Control (5% sucrose, orally) daily for 12 weeks; (2) ethanol (4 g kg(-1), orally) daily for 12 weeks; (3) exercise training on treadmill plus sucrose daily for 12 weeks and (4) exercise training on treadmill followed by ethanol (4 g kg(-1), orally) daily for 12 weeks. The body weight, BP and HR were recorded every week. The animals were sacrificed under ether anesthesia after 12 weeks, blood collected in heparinzed vials, plasma isolated and analyzed. The results show that exercise training significantly lowered the weight gain 6-12 weeks in ethanol treated rats compared to ethanol alone or control rats. The mean arterial BP was significantly elevated 6-12 weeks after ethanol ingestion without significant alterations in HR. Exercise training lowered the BP close to the normal control values in ethanol fed rats. Ethanol significantly decreased the plasma NO levels, reduced to oxidized glutathione ratio (GSH/GSSG) and antioxidant enzymes-superoxide dismutase (CuZn-SOD, and Mn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities while plasma NADPH oxidase activity and malondialdehyde (MDA) levels were significantly elevated compared to control. Exercise training significantly restored the depletion of plasma NO levels, GSH/GSSG ratio, and antioxidant enzyme activities and normalized the MDA levels and NADPH oxidase activity in the plasma of ethanol treated rats. The study concluded that physical conditioning attenuates the chronic ethanol-induced hypertension by augmenting the NO bioavailability and reducing the oxidative stress response in the plasma of rats.

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Effects of chronic ethanol consumption on α-adrenergic-induced contractions in rat thoracic aorta

Cited by 40 publications

References 17 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

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

Physiological basis for effect of physical conditioning on chronic ethanol-induced hypertension in a rat model

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