Key result
Acoustic stress increased sympathetic innervation in the rat cardiovascular system and modified the maximal response of beta-adrenoceptors, suggesting changes in postreceptorial mechanisms.
Noise stress increases sympathetic innervation and alters postreceptorial mechanisms of beta-adrenoceptors in the rat cardiovascular system.
Environmental noise may influence cardiac sympathetic signaling; leaves open translation to human cardiovascular risk.
One, six and twelve hs of exposure to acoustic stress showed different influences on the noradrenergic pattern and receptor function of the rat atria and aorta. Moreover, the lipid content of the adrenal cortex and hepatic glycogen were histochemically evaluated in the same animals to correlate these observations with the previous results. The increase in exposure time induced a corresponding increase in sympathetic innervation, which was more evident at cardiac level. The functional results showed that the potency of the agonists on the alpha- and beta-adrenoceptors does not vary, with the exception of 6-h treatment, which affected beta-receptors. By contrast, the M.R.R. of beta-receptors proved to be modified in all treatments, suggesting that noise stress affected mainly postreceptorial mechanisms linked to beta-adrenoceptors rather than their density or affinity; no significant functional modifications were observed when alpha-receptors were considered.
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Breschi et al. (1994) studied Acoustic stress. Acoustic stress was evaluated on Noradrenergic pattern and receptor function of the atria and aorta. Acoustic stress increased sympathetic innervation in the rat cardiovascular system and modified the maximal response of beta-adrenoceptors, suggesting changes in postreceptorial mechanisms.
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