Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth hormone secretagogues (GHSs) increase the activity of hypothalamic arcuate nucleus neurons thought to be involved in controlling the release of growth hormone (GH). The GHS receptor is also found in hypothalamic regions not associated with the release of GH, suggesting that GHSs may influence other hypothalamic systems. This study utilized double-labeling immunocytochemical techniques to examine the hypothalamic actions of a novel nonpeptide GHS, GHS-25. In common with other GHSs, GHS-25 induced significant amounts of Fos immunoreactivity in the arcuate nucleus of conscious male rats. However, unlike other GHSs, GHS-25 also induced Fos immunoreactivity in the supraoptic nucleus. Double labeling revealed that approx 66% of supraoptic nucleus cells that were Fos positive after the administration of GHS-25 were also immunoreactive for oxytocin. Thus, in addition to its actions on the GH axis, GHS-25 may influence the release of neurohypophyseal hormone.
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PMID:Central actions of the nonpeptide growth hormone secretagogue GHS-25. 1132 97

Growth hormone (GH)-releasing peptides (GHRPs) are synthetic peptides that strongly induce GH release. GHRPs act via a specific receptor, the GHRP receptor (GHSR), of which ghrelin is a natural ligand. GHRPs also induce adrenocorticotropic hormone (ACTH) release in healthy subjects. GHRPs or ghrelin stimulate ACTH release via corticotropin-releasing factor (CRF) and arginin vasopressin in the hypothalamus. Stress-activated CRF neurons are suppressed by glucocorticoids in the hypothalamic paraventricular nucleus (PVN), while CRF gene is up-regulated by glucocorticoids in the PVN cells without the influence of input neurons. However, little is known about the regulation of ghrelin and GHSR type 1a (GHSR1a) genes by glucocorticoids in PVN cells. To elucidate the regulation of ghrelin and GHSR gene expression by glucocorticoids in PVN cells, here we used a homologous PVN neuronal cell line, hypothalamic 4B, because these cells show characteristics of the parvocellular neurons of the PVN. These cells also express ghrelin and GHSR1a mRNA. Dexamethasone increased ghrelin mRNA levels. A potent glucocorticoid receptor antagonist, RU-486, significantly blocked dexamethasone-induced increases in ghrelin mRNA levels. Dexamethasone also significantly stimulated GHSR1a mRNA and protein levels. Finally, ghrelin increased CRF mRNA levels, as did dexamethasone. Incubation with both dexamethasone and ghrelin had an additive effect on CRF and ghrelin mRNA levels. The ghrelin-GHSR1a system is activated by glucocorticoids in the hypothalamic cells.
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PMID:Dexamethasone stimulates the expression of ghrelin and its receptor in rat hypothalamic 4B cells. 2212 Aug 31

Traumatic brain injury(TBI)is a major cause of hypothalamopituitary dysfunction. TBI-related hypothalamopituitary dysfunction is more common in the acute phase. Disturbance of pituitary/gonadal axis and growth hormone axis,as well as posterior pituitary dysfunction including central diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion,are the most frequently seen. During the chronic phase of TBI,anterior hypopituitarism is the major concern,which affects the quality of life. Risk factors for hypothalamopituitary dysfunction following TBI include low Glasgow score,high body mass index,hypoxia,older age,longer intensive care unit stay and longer coma status,radiological evidence of acute brain injury,and increased intracranial pressure. Children and adolescents are in a crucial period of growth and development,and therefore TBI-related pituitary dysfunction during this period can substantially affect the cognition and behaviors. There is currently no reliable biochemical marker predicting hypothalamopituitary dysfunctions. Therefore,it is of great importance to evaluate the pituitary function and take appropriate hormone replacement for moderate-severe TBI patients or mild TBI patients with apparent symptoms,especially for patients with water-electrolyte disturbance and adrenal deficiency. Growth hormone and gonadal hormone replacement therapies are crucial for children and adolescents.
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PMID:[Research Advances in Hypothalamic-pituitary Dysfunction Related to Traumatic Brain Injury]. 3040 5


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