Source:http://linkedlifedata.com/resource/pubmed/id/21470318
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2011-5-13
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pubmed:abstractText |
Secretion of vasopressin (VP), oxytocin (OT) and atrial natriuretic peptide (ANP) is an essential mechanism for the maintenance of hydromineral homeostasis. Secretion of these hormones is modulated by several circulating factors, including oestradiol. However, it remains unclear how oestradiol exerts this modulation. In the present study we investigated the participation of oestradiol in the secretion of VP, OT and ANP and in activation of vasopressinergic and oxytocinergic neurones of the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus in response to extracellular volume expansion (EVE). For this purpose, ovariectomised (OVX) rats treated for 7?days with vehicle (corn oil, 0.1?ml/rat, OVX+O group) or oestradiol (oestradiol cypionate, 10??g/kg, OVX+E group) were subjected to either isotonic (0.15?m NaCl, 2?ml/100?g b.w., i.v.) or hypertonic (0.30?m NaCl, 2?ml/100?g b.w., i.v.) EVE. Blood samples were collected for plasma VP, OT and ANP determination. Another group of rats was subjected to cerebral perfusion, and brain sections were processed for c-Fos-VP and c-Fos-OT double-labelling immunohistochemistry. In OVX+O rats, we observed that both isotonic and hypertonic EVE increased plasma OT and ANP concentrations, although no changes were observed in VP secretion. Oestradiol replacement did not alter hormonal secretion in response to isotonic EVE, but it increased VP secretion and potentiated plasma OT and ANP concentrations in response to hypertonic EVE. Immunohistochemical data showed that, in the OVX+O group, hypertonic EVE increased the number of c-Fos-OT and c-Fos-VP double-labelled neurones in the PVN and SON. Oestradiol replacement did not alter neuronal activation in response to isotonic EVE, but it potentiated vasopressinergic and oxytocinergic neuronal activation in the medial magnocellular PVN (PaMM) and SON. Taken together, these results suggest that oestradiol increases the responsiveness of vasopressinergic and oxytocinergic magnocellular neurones in the PVN and SON in response to osmotic stimulation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Arginine Vasopressin,
http://linkedlifedata.com/resource/pubmed/chemical/Estradiol,
http://linkedlifedata.com/resource/pubmed/chemical/Hormones,
http://linkedlifedata.com/resource/pubmed/chemical/Hypertonic Solutions,
http://linkedlifedata.com/resource/pubmed/chemical/Oxytocin,
http://linkedlifedata.com/resource/pubmed/chemical/Vasopressins
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1365-2826
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pubmed:author | |
pubmed:copyrightInfo |
© 2011 The Authors. Journal of Neuroendocrinology © 2011 Blackwell Publishing Ltd.
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pubmed:issnType |
Electronic
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
481-9
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pubmed:meshHeading |
pubmed-meshheading:21470318-Animals,
pubmed-meshheading:21470318-Arginine Vasopressin,
pubmed-meshheading:21470318-Cell Size,
pubmed-meshheading:21470318-Estradiol,
pubmed-meshheading:21470318-Extracellular Fluid,
pubmed-meshheading:21470318-Female,
pubmed-meshheading:21470318-Hormones,
pubmed-meshheading:21470318-Hypertonic Solutions,
pubmed-meshheading:21470318-Neurons,
pubmed-meshheading:21470318-Ovariectomy,
pubmed-meshheading:21470318-Oxytocin,
pubmed-meshheading:21470318-Rats,
pubmed-meshheading:21470318-Rats, Wistar,
pubmed-meshheading:21470318-Secretory Pathway,
pubmed-meshheading:21470318-Synaptic Transmission,
pubmed-meshheading:21470318-Up-Regulation,
pubmed-meshheading:21470318-Vasopressins
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pubmed:year |
2011
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pubmed:articleTitle |
Oestradiol potentiates hormone secretion and neuronal activation in response to hypertonic extracellular volume expansion in ovariectomised rats.
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pubmed:affiliation |
Departamento de Fisiologia, Faculdade de Medicina de Ribeirao Preto, Universidade de Sao Paulo, Brasil.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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