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Neuronal Fos-like immunoreactivity associated with dexamethasone-induced hypertension in rats and effects of glucagon-like peptide-2

Authors
Journal
Life Sciences
0024-3205
Publisher
Elsevier
Publication Date
Volume
93
Issue
23
Identifiers
DOI: 10.1016/j.lfs.2013.10.016
Keywords
  • Dexamethasone
  • C-Fos Protein
  • Blood Pressure
  • Hypothalamus
  • Glp-2
Disciplines
  • Biology
  • Chemistry
  • Medicine

Abstract

Abstract Aims Dexamethasone-induced hypertension models have been used to study the mechanisms of glucocorticoid-induced hypertension, but the role of glucocorticoids in central cardiovascular regulation is not clearly understood. In the present study, we investigated the sites associated with dexamethasone-induced hypertension in the central nervous system in rats. We further investigated whether glucagon-like peptide-2 (GLP-2) was effective for dexamethasone-induced hypertension. Main methods Male Sprague–Dawley rats were treated with saline or dexamethasone (0.03mg/kg/day, s.c) for 10days. GLP-2 (60μg/kg, i.v.) was given to rats after dexamethasone treatment. We measured systolic blood pressure by a tail-cuff method in conscious rats, and arterial blood pressure in anesthetized rats. Immunohistochemical techniques were used to detection of the c-fos protein (Fos). Key findings Fos-immunoreactivity (Fos-IR) in the dorsomedial hypothalamic nucleus (DMH) was higher in dexamethasone-treated rats than in saline-treated rats. However, Fos-IR in the infralimbic cortex, amygdala, and hippocampus was similar in saline-treated and dexamethasone-treated rats. Peripheral administration of GLP-2 reduced mean arterial blood pressure by 26%. After the peripheral administration of GLP-2, Fos-IR in the caudal ventrolateral medulla (CVLM) increased in dexamethasone-treated rats. Significance Chronic dexamethasone treatment induced Fos-IR in the DMH. Peripheral administration of GLP-2 suppressed dexamethasone-induced hypertension in rats by enhancing inhibitory neuronal activity.

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