Key result
Chronic immobilization stress increased rat aortic maximum contractile responses to noradrenaline, an effect dependent on the vascular endothelium and release of vasoconstrictor prostanoids via alpha-2 adrenoceptors, whereas chronic ethanol consumption had no effect.
Why the study?
Does chronic stress and/or ethanol consumption alter aortic reactivity to sympathetic agonists in adult male rats?
Does chronic stress and/or ethanol consumption alter aortic reactivity to sympathetic agonists in adult male rats?
p-value: p=<0.05
Chronic stress induces aortic hyper-reactivity to noradrenaline via endothelial alpha-2 adrenoceptor stimulation and vasoconstrictor prostanoid release, an effect not modified by chronic ethanol consumption.
No direct clinical implications from rat data; leaves open whether endothelial prostanoids mediate stress effects on human vascular reactivity.
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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Baptista et al. (2014) studied Cardiovascular risk (animal model). Immobilization stress and/or 20% ethanol vs. Control (water ad libitum, no stress) was evaluated on Maximum response (Rmax) to noradrenaline in intact thoracic aortas (p=<0.05). Chronic immobilization stress increased rat aortic maximum contractile responses to noradrenaline, an effect dependent on the vascular endothelium and release of vasoconstrictor prostanoids via alpha-2 adrenoceptors, whereas chronic ethanol consumption had no effect.
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