BackgroundStress and ethanol are both, independently, important cardiovascular risk
factors.ObjectiveTo evaluate the cardiovascular risk of ethanol consumption and stress exposure,
isolated and in association, in male adult rats.MethodsRats 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.ResultsEither 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.ConclusionChronic 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.