Abstract
Arginin vasopressin (AVP) as well as corticotropin-releasing hormone (CRH) is well known to modulate ACTH release from the anterior pituitary gland via V1b receptor. The parvocellular neurosecretory cells in the paraventricular nucleus (PVN) of the hypothalamus synthesize AVP and CRH, project their axons to the external layer of the median eminence (ME) and secrete AVP and CRH into the portal blood flow. The synthesis and secretion of AVP and CRH are modulated by various stressors. We examined the effects of adrenalectomy (ADX), endotoxin shock and chronic inflammatory stress on the expression of AVP and CRH in the PVN of rats. In AVP-enhanced green fluorescent protein (eGFP) transgenic rats eGFP was marked increased in the external layer of the ME and the parvocellular CRH-producing neurons of the PVN 5 days after bilateral ADX. After acute and chronic inflammatory stress one of novel G-protein coupled receptor ligands, galanin-like peptide (GALP), expressed in the pituicytes of the posterior pituitary gland. In in vitro preparation GALP stimulated AVP release from the posterior pituitary. During chronic inflammatory stress such as adjuvant arthritis the expression of the AVP gene in the PVN was upregulated, while the expression of the CRH gene in the PVN was downregulated. These results suggest that AVP and CRH in the PVN may have different regulatory mechanism under acute and chronic inflammatory stress. The monitoring the eGFP expression in the PVN and the ME in AVP-eGFP transgenic rats may give us new information about the physiological role of central AVP system under acute and chronic stress. [Jpn J Physiol 55 Suppl:S16 (2005)]
