Source:http://linkedlifedata.com/resource/pubmed/id/10414997
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001655,
umls-concept:C0003779,
umls-concept:C0010124,
umls-concept:C0010132,
umls-concept:C0020663,
umls-concept:C0030532,
umls-concept:C0030685,
umls-concept:C0039601,
umls-concept:C0085862,
umls-concept:C0185027,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1280500,
umls-concept:C1283071,
umls-concept:C1299583,
umls-concept:C1515670,
umls-concept:C1549571,
umls-concept:C1608386,
umls-concept:C1963578
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pubmed:issue |
15
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pubmed:dateCreated |
1999-8-16
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pubmed:abstractText |
Adrenocorticotropin (ACTH) release is regulated by both glucocorticoids and androgens; however, the precise interactions are unclear. We have controlled circulating corticosterone (B) and testosterone (T) by adrenalectomy (ADX) +/- B replacement and gonadectomy (GDX) +/- T replacement, comparing these to sham-operated groups. We hoped to reveal how and where these neuroendocrine systems interact to affect resting and stress-induced ACTH secretion. ADX responses. In gonadal-intact rats, ADX increased corticotropin-releasing factor (CRH) and vasopressin (AVP) mRNA in hypothalamic parvocellular paraventricular nuclei (PVN) and ACTH in pituitary and plasma. B restored these toward normal. GDX blocked the increase in AVP but not CRH mRNA and reduced plasma, but not pituitary ACTH in ADX rats. GDX+T restored increased AVP mRNA in ADX rats, although plasma ACTH remained decreased. Stress responses. Restraint-induced ACTH responses were elevated in ADX gonadally intact rats, and B reduced these toward normal. GDX in adrenal-intact and ADX+B rats increased ACTH responses. Without B, T did not affect ACTH; together with B, T restored ACTH responses to normal. The magnitude of ACTH responses to stress was paralleled by similar effects on the number of c-fos staining neurons in the hypophysiotropic PVN. We conclude that gonadal regulation of ACTH responses to ADX is determined by T dependent effects on AVP biosynthesis, whereas CRH biosynthesis is B-dependent. Stress-induced ACTH release is not explained by B and T interactions at the PVN, but is determined by B- and T-dependent changes in drive to PVN motorneurons.
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pubmed:grant | |
pubmed:keyword | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenocorticotropic Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Arginine Vasopressin,
http://linkedlifedata.com/resource/pubmed/chemical/Corticosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Corticotropin-Releasing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-fos,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Testosterone
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0270-6474
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
19
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6684-93
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10414997-Adrenalectomy,
pubmed-meshheading:10414997-Adrenocorticotropic Hormone,
pubmed-meshheading:10414997-Animals,
pubmed-meshheading:10414997-Arginine Vasopressin,
pubmed-meshheading:10414997-Corticosterone,
pubmed-meshheading:10414997-Corticotropin-Releasing Hormone,
pubmed-meshheading:10414997-Male,
pubmed-meshheading:10414997-Paraventricular Hypothalamic Nucleus,
pubmed-meshheading:10414997-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:10414997-RNA, Messenger,
pubmed-meshheading:10414997-Rats,
pubmed-meshheading:10414997-Rats, Sprague-Dawley,
pubmed-meshheading:10414997-Restraint, Physical,
pubmed-meshheading:10414997-Stress, Physiological,
pubmed-meshheading:10414997-Testosterone
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pubmed:year |
1999
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pubmed:articleTitle |
Independent and overlapping effects of corticosterone and testosterone on corticotropin-releasing hormone and arginine vasopressin mRNA expression in the paraventricular nucleus of the hypothalamus and stress-induced adrenocorticotropic hormone release.
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pubmed:affiliation |
Department of Physiology, University of California at San Francisco, San Francisco, California 94143, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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