Why the study?
Does sinoaortic denervation increase cardiovascular and endocrine responses to acute stress in male Sprague-Dawley rats?
Does sinoaortic denervation increase cardiovascular and endocrine responses to acute stress in male Sprague-Dawley rats?
Sinoaortic denervation does not uniformly exaggerate centrally derived cardiovascular and endocrine responses to acute stress in a rat model.
No immediate clinical implications from this rat model; leaves open baroreflex contributions to human cardiovascular reactivity.
Sinoaortic baroreceptor denervation is reported to produce exaggerated centrally derived cardiovascular and endocrine responses. We examined the effect of sinoaortic denervation (SAD) on the cardiovascular and endocrine responses to two acute stressors, footshock and immobilization, in male Sprague-Dawley rats. Parameters measured were mean arterial pressure (MAP), heart rate (HR) and plasma levels of oxytocin (OT) and vasopressin (VP). Baseline MAP was elevated in the SAD group (approximately 25 mm Hg) and footshock stress increased arterial pressure equivalently in both groups. This stress caused tachycardia and increased plasma OT, with a tendency for the SAD group to show blunted responses. Immobilization increased HR but caused no change in MAP and no significant difference between the groups. This form of stress also increased plasma OT, and again the SAD group showed a diminished response. Plasma VP was not significantly altered by either stressor. The results of these studies indicate that SAD does not uniformly increase the cardiovascular and endocrine responses to all stressors or centrally derived stimuli. These results also suggest that the lack of an increase in plasma VP is not related to baroreceptor-mediated inhibition of secretion under stressful conditions.
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Callahan et al. (2008) studied this question.
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