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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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Plasma concentration of nitrite/nitrate determined by the Griess Reaction takenfrom animals exposed to ethanol consumption and/or stress. Values are expressed asmeans ± SEM. The number of independent determinations was 10-12.
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f08: Plasma concentration of nitrite/nitrate determined by the Griess Reaction takenfrom animals exposed to ethanol consumption and/or stress. Values are expressed asmeans ± SEM. The number of independent determinations was 10-12.

Mentions: The concentration in plasma of nitrite/nitrate, determined by the Griess Reaction, wasnot significantly different among groups (Figure4).


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)

Plasma concentration of nitrite/nitrate determined by the Griess Reaction takenfrom animals exposed to ethanol consumption and/or stress. Values are expressed asmeans ± SEM. The number of independent determinations was 10-12.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f08: Plasma concentration of nitrite/nitrate determined by the Griess Reaction takenfrom animals exposed to ethanol consumption and/or stress. Values are expressed asmeans ± SEM. The number of independent determinations was 10-12.
Mentions: The concentration in plasma of nitrite/nitrate, determined by the Griess Reaction, wasnot significantly different among groups (Figure4).

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