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Acta physiol. pharmacol. ther. latinoam ; 49(2): 71-8, 1999. tab, graf
Article in English | LILACS | ID: lil-245921

ABSTRACT

The limbic structures play an important role in the control of the neuroendocrine and sympathical adrenal function in basal and stress conditions. This work was undertaken to evaluate plasma ACTH, adrenocortical activity, cardiac adrenoceptors density and affnity response to variable chronic stress (VCS) in anterodorsal thalamic nuclei (ADTN) lesioned rats. Thirty days after lesion, shamlesioned stressed animals increased plasma ACTH and corticosterone as compared to sham-lesioned unstressed animals (p<0.05); lesioned rats increased ACTH levels after VCS (p<0.05) as compared unstressed-lesioned rats. Whereas in sham-lesion plasma corticosterone (C) increased after stress. in lesioned animals (C) remained unchanged as compared to unstressed-lesioned animals. In the stressed groups, adrenal C contents were below those found in unstressed rats. Beta-receptors affinity, in all the experimental groups, was similar, but VCS sham-lesioned animals underwent a significant increase in cardiac D-adrenergic receptors density when compared with basal and lesioned groups (P<0.001). Our findings would demonstrate that the increment in cardiac Beta adrenoceptors density appears as a consequence of the increase in ACTH, plasma corticosterone and sympathetic response provoked by stress situations. ADTN lesion attenuated this hipophisoadrenal system response to chronic stress as well as the above mentioned cardiac beta adrenoceptors density increment.


Subject(s)
Animals , Female , Rats , Adrenocorticotropic Hormone/blood , Corticosterone/blood , Heart Ventricles/pathology , Pituitary-Adrenal System/pathology , Receptors, Adrenergic, beta/physiology , Stress, Physiological/physiopathology , Thalamic Nuclei/pathology , Adrenocorticotropic Hormone/metabolism , Analysis of Variance , Chronic Disease , Corticosterone/metabolism , Disease Models, Animal , Heart Ventricles/pathology , Rats, Wistar , Receptors, Adrenergic, beta/metabolism , Thalamic Nuclei/pathology
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