Sinoaortic Denervation Does Not Increase Cardiovascular/ Endocrine Responses to Stress

Abstract

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 (≈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.

Neuroendocrine responses to an emotional stressor: evidence for involvement of the medial but not the central amygdala

“…In animals subjected to restraint, we observed patterns of hypothalamic neuroendocrine cell c‐ fos expression consistent with existing evidence that, like other emotional stressors, this stimulus activates the HPA axis and enhances OT release, but not VP release ( Lang et al . 1983 ; Gibbs 1984; Carter & Lightman 1987; Callahan et al . 1992 ).…”

Sinoaortic Denervation Alters the Molecular and Endocrine Responses to Salt Loading

“…In addition to changes in basal peptide levels, the SAD ani mals show an elevation in osmotic responsiveness as tested with intravenous hypertonic saline [19]. This was not a generalized phenomenon since there were no alter ations in stress or hemorrhage-induced hormone secre tion after baroreceptor denervation [3,5,7].…”

“…The changes in basal plasma and central ner vous system peptides are most noticeable in the early postoperative period while the alterations in osmotic responsiveness are more long-lasting. The endocrine changes appear to be specific for the salt stimulus since there were no alterations in stress or hemorrhage-induced peptide release [3,5,7]. It is likely that the baroreceptor nerves exert their influence indirectly via input from the brain stem although the exact mechanisms are not known.…”

β-Adrenoceptors in the medial amygdaloid nucleus modulate the tachycardiac response to restraint stress in rats

“…In addition, the response to stress is characterized by an increased circulating content of the corticotropin-releasing hormone (CRH), which plays an important role in the secretion of adrenocorticotropin (ACTH) and corticosteroid (Harbuz et al, 1992). The restraint stress has been reported to activate the hypothalamicpituitary-adrenal (HPA) axis and to cause oxytocin release, but not the release of vasopressin (Lang et al, 1983;Gibbs, 1984;Carter and Lightman, 1987;Callahan et al, 1992;Dayas et al, 1999). Data from the literature also indicate a larger activation of the MeA, among other amygdaloid nuclei, during stressful situations, as indicated by the large expression of c-Fos protein in this area after the exposure to aversive situations (Canteras et al, 1995;Chen and Herbert, 1995;Cullinan et al, 1995;Dayas et al, 1999;Dayas et al, 2001aDayas et al, , 2001bKubo et al, 2004;Crane et al, 2005;Trneckova et al, 2006).…”