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Stress alone or associated with ethanol induces prostanoid release in rat aorta via alpha2-Adrenoceptor.

Baptista Rde F, Taipeiro Ede F, Queiroz RH, Chies AB, Cordellini S - Arq. Bras. Cardiol. (2014)

Bottom Line: EC50 and maximum response (n=8-12) were compared using two-way ANOVA/Bonferroni method.Meanwhile, ethanol consumption did not alter the reactivity to noradrenaline.This effect is dependent upon the vascular endothelium and involves the release of vasoconstrictor prostanoids via stimulation of endothelial alpha-2 adrenoceptors.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Farmacologia, Instituto de Biociências, Universidade Estadual Paulista, São Paulo, SP, Brasil.

ABSTRACT

Background: Stress and ethanol are both, independently, important cardiovascular risk factors.

Objective: To evaluate the cardiovascular risk of ethanol consumption and stress exposure, isolated and in association, in male adult rats.

Methods: Rats were separated into 4 groups: Control, ethanol (20% in drinking water for 6 weeks), stress (immobilization 1h day/5 days a week for 6 weeks) and stress/ethanol. Concentration-responses curves to noradrenaline - in the absence and presence of yohimbine, L-NAME or indomethacin - or to phenylephrine were determined in thoracic aortas with and without endothelium. EC50 and maximum response (n=8-12) were compared using two-way ANOVA/Bonferroni method.

Results: Either stress or stress in association with ethanol consumption increased the noradrenaline maximum responses in intact aortas. This hyper-reactivity was eliminated by endothelium removal or by the presence of either indomethacin or yohimbine, but was not altered by the presence of L-NAME. Meanwhile, ethanol consumption did not alter the reactivity to noradrenaline. The phenylephrine responses in aortas both with and without endothelium also remained unaffected regardless of protocol.

Conclusion: Chronic stress increased rat aortic responses to noradrenaline. This effect is dependent upon the vascular endothelium and involves the release of vasoconstrictor prostanoids via stimulation of endothelial alpha-2 adrenoceptors. Moreover, chronic ethanol consumption appeared to neither influence noradrenaline responses in rat thoracic aorta, nor did it modify the increase of such responses observed as a consequence of stress exposure.

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Related in: MedlinePlus

Concentration-response curves to noradrenaline obtained from intact thoracic aortarings taken from animals exposed to ethanol consumption and/or stress, in theabsence or presence of L-NAME (10-4 M), indomethacin (10-5M) or yohimbine (10-6 M). Values are expressed as means ± SEM.The number of independent determinations was 8-10. *Indicates a significantdifference (p < 0.05) in relation to the control animals.
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f05: Concentration-response curves to noradrenaline obtained from intact thoracic aortarings taken from animals exposed to ethanol consumption and/or stress, in theabsence or presence of L-NAME (10-4 M), indomethacin (10-5M) or yohimbine (10-6 M). Values are expressed as means ± SEM.The number of independent determinations was 8-10. *Indicates a significantdifference (p < 0.05) in relation to the control animals.

Mentions: The noradrenaline responses observed in intact aortas taken from animals exposed to bothstress and stress/ethanol in combination, were higher than those observed in intactaortas taken from control animals. These outcomes resulted in increased values ofRmax. Animals exposed to ethanol alone, however, did not demonstratehigher responses than controls (Figure 1A). Thepresence of L-NAME increased the noradrenaline Rmax in aortic rings takenfrom control and ethanol groups, permitting responses of similar magnitude withpreparations taken from stress and stress/ethanol groups (Figures 1B). Inversely, indomethacin abolished the elevation of noradrenalineresponses in aortas from stress and stress/ethanol groups, thereby resulting in valuesof Rmax at the level of the control group (Figure 1C). Similarly, yohimbine also abolished the hyper-reactivity tonoradrenaline in thoracic aorta taken from stress and stress/ethanol animals (Figure 1D). Finally, regarding EC50, nodifferences were detected among groups regardless of absence or presence of L-NAME,indomethacin or yohimbine (Table 1).


Stress alone or associated with ethanol induces prostanoid release in rat aorta via alpha2-Adrenoceptor.

Baptista Rde F, Taipeiro Ede F, Queiroz RH, Chies AB, Cordellini S - Arq. Bras. Cardiol. (2014)

Concentration-response curves to noradrenaline obtained from intact thoracic aortarings taken from animals exposed to ethanol consumption and/or stress, in theabsence or presence of L-NAME (10-4 M), indomethacin (10-5M) or yohimbine (10-6 M). Values are expressed as means ± SEM.The number of independent determinations was 8-10. *Indicates a significantdifference (p < 0.05) in relation to the control animals.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3987321&req=5

f05: Concentration-response curves to noradrenaline obtained from intact thoracic aortarings taken from animals exposed to ethanol consumption and/or stress, in theabsence or presence of L-NAME (10-4 M), indomethacin (10-5M) or yohimbine (10-6 M). Values are expressed as means ± SEM.The number of independent determinations was 8-10. *Indicates a significantdifference (p < 0.05) in relation to the control animals.
Mentions: The noradrenaline responses observed in intact aortas taken from animals exposed to bothstress and stress/ethanol in combination, were higher than those observed in intactaortas taken from control animals. These outcomes resulted in increased values ofRmax. Animals exposed to ethanol alone, however, did not demonstratehigher responses than controls (Figure 1A). Thepresence of L-NAME increased the noradrenaline Rmax in aortic rings takenfrom control and ethanol groups, permitting responses of similar magnitude withpreparations taken from stress and stress/ethanol groups (Figures 1B). Inversely, indomethacin abolished the elevation of noradrenalineresponses in aortas from stress and stress/ethanol groups, thereby resulting in valuesof Rmax at the level of the control group (Figure 1C). Similarly, yohimbine also abolished the hyper-reactivity tonoradrenaline in thoracic aorta taken from stress and stress/ethanol animals (Figure 1D). Finally, regarding EC50, nodifferences were detected among groups regardless of absence or presence of L-NAME,indomethacin or yohimbine (Table 1).

Bottom Line: EC50 and maximum response (n=8-12) were compared using two-way ANOVA/Bonferroni method.Meanwhile, ethanol consumption did not alter the reactivity to noradrenaline.This effect is dependent upon the vascular endothelium and involves the release of vasoconstrictor prostanoids via stimulation of endothelial alpha-2 adrenoceptors.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Farmacologia, Instituto de Biociências, Universidade Estadual Paulista, São Paulo, SP, Brasil.

ABSTRACT

Background: Stress and ethanol are both, independently, important cardiovascular risk factors.

Objective: To evaluate the cardiovascular risk of ethanol consumption and stress exposure, isolated and in association, in male adult rats.

Methods: Rats were separated into 4 groups: Control, ethanol (20% in drinking water for 6 weeks), stress (immobilization 1h day/5 days a week for 6 weeks) and stress/ethanol. Concentration-responses curves to noradrenaline - in the absence and presence of yohimbine, L-NAME or indomethacin - or to phenylephrine were determined in thoracic aortas with and without endothelium. EC50 and maximum response (n=8-12) were compared using two-way ANOVA/Bonferroni method.

Results: Either stress or stress in association with ethanol consumption increased the noradrenaline maximum responses in intact aortas. This hyper-reactivity was eliminated by endothelium removal or by the presence of either indomethacin or yohimbine, but was not altered by the presence of L-NAME. Meanwhile, ethanol consumption did not alter the reactivity to noradrenaline. The phenylephrine responses in aortas both with and without endothelium also remained unaffected regardless of protocol.

Conclusion: Chronic stress increased rat aortic responses to noradrenaline. This effect is dependent upon the vascular endothelium and involves the release of vasoconstrictor prostanoids via stimulation of endothelial alpha-2 adrenoceptors. Moreover, chronic ethanol consumption appeared to neither influence noradrenaline responses in rat thoracic aorta, nor did it modify the increase of such responses observed as a consequence of stress exposure.

Show MeSH
Related in: MedlinePlus