| pubmed-article:3138865 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3138865 | lifeskim:mentions | umls-concept:C2250368 | lld:lifeskim |
| pubmed-article:3138865 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:3138865 | pubmed:dateCreated | 1988-10-24 | lld:pubmed |
| pubmed-article:3138865 | pubmed:abstractText | The secretion of FSH appears to be dominated by factors controlling the inhibition of synthesis and release acting directly at the level of the gonadotrope in the pituitary. Only minimal amounts of GnRH are necessary to stimulate and maintain the secretion of FSH, and, in contrast to LH, the release of FSH is closely linked to the rate of synthesis. Estradiol is a potent inhibitor of FSH release acting directly at the gonadotrope to inhibit mRNA transcription. In vivo, estradiol alone in physiological concentrations cannot maintain plasma concentrations within the normal levels seen during the estrus or menstrual cycle. It is probable that estradiol acts synergistically with inhibin both of which are secreted by the developing follicle. Inhibin secretion in the follicle is dependent on FSH. During the follicular phase in sheep and women peripheral plasma concentrations of inhibin remain unchanged or decline in parallel with those of FSH, and inversely to estradiol. In the luteal phase, the human corpus luteum secretes inhibin under the influence of LH. Thus inhibin together with both estradiol and progesterone secreted by the corpus luteum, accounts for the suppression of FSH and thus follicular development in the luteal phase of the human menstrual cycle. | lld:pubmed |
| pubmed-article:3138865 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3138865 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3138865 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:3138865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:3138865 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3138865 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3138865 | pubmed:issn | 0300-9750 | lld:pubmed |
| pubmed-article:3138865 | pubmed:author | pubmed-author:McNeillyA SAS | lld:pubmed |
| pubmed-article:3138865 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3138865 | pubmed:volume | 288 | lld:pubmed |
| pubmed-article:3138865 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3138865 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3138865 | pubmed:pagination | 31-40 | lld:pubmed |
| pubmed-article:3138865 | pubmed:dateRevised | 2008-2-12 | lld:pubmed |
| pubmed-article:3138865 | pubmed:meshHeading | pubmed-meshheading:3138865-... | lld:pubmed |
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| pubmed-article:3138865 | pubmed:meshHeading | pubmed-meshheading:3138865-... | lld:pubmed |
| pubmed-article:3138865 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:3138865 | pubmed:articleTitle | The control of FSH secretion. | lld:pubmed |
| pubmed-article:3138865 | pubmed:affiliation | MRC Reproductive Biology Unit, Edinburg, Scotland. | lld:pubmed |
| pubmed-article:3138865 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3138865 | pubmed:publicationType | Review | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:3138865 | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:3138865 | lld:pubmed |
