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Heart rate (HR) and blood pressure responses to nonsignal auditory stimuli were measured in rats after saline or pharmacological blockade of the sympathetic or vagal innervation of the heart. HR responses to the low-intensity stimulus were predominantly deceleratory, whereas responses to the high-intensity stimulus were more notably acceleratory. Both stimuli elicited a biphasic pressor-depressor response, although potential baroreflex influences accounted for only a small proportion of the HR response variance. Deceleratory responses to the low-intensity stimulus were eliminated by scopolamine and thus appeared to be predominantly of vagal origin. Acceleratory response to the high-intensity stimulus appeared to be mediated primarily by sympathetic activation because it was substantially attenuated by the beta 1 antagonist atenolol. Furthermore, HR responses to the low-intensity stimulus appeared to reflect coactivation of both sympathetic and vagal systems.
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Quigley et al. (1990) studied this question.
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