PMID- 15512850
OWN - NLM
STAT- MEDLINE
DCOM- 20041209
LR  - 20081121
IS  - 1025-3890 (Print)
IS  - 1025-3890 (Linking)
VI  - 7
IP  - 2
DP  - 2004 Jun
TI  - Vasopressinergic regulation of the hypothalamic pituitary adrenal axis and stress 
      adaptation.
PG  - 75-83
AB  - Vasopressin (VP) stimulates pituitary ACTH secretion through interaction with 
      receptors of the V1b subtype (V1bR, V3R), located in the plasma membrane of the 
      pituitary corticotroph, mainly by potentiating the stimulatory effects of 
      corticotropin releasing hormone (CRH). Chronic stress paradigms associated with 
      corticotroph hyperresponsiveness lead to preferential expression of hypothalamic 
      VP over CRH and upregulation of pituitary V1bR, suggesting an important role for 
      VP during adaptation of the hypothalamic-pituitary-adrenal (HPA) axis to stress. 
      Vasopressinergic regulation of ACTH secretion depends on the number of V1bRs as 
      well as coupling of the receptor to phospholipase C (PLC) in the pituitary. 
      Regulation of V1bR gene transcription may involve a number of regulatory elements 
      in the promoter region, of which a GAGA box was shown to be essential. Although 
      V1bR gene transcription is necessary to maintain V1bR mRNA levels, the lack of 
      correlation between VP binding and V1bR mRNA suggests that regulation of mRNA 
      translation is a major regulatory step of the number of V1bRs. V1bR translation 
      appears to be under tonic inhibition by upstream minicistrons and positive 
      regulation through protein kinase C (PKC) activation of an internal ribosome 
      entry site (IRES) in the 5' untranslated region (5'UTR) of the mRNA. The data 
      provide mechanisms by which regulation of hypothalamic VP and pituitary V1bR 
      content contribute to controlling HPA axis activity during chronic stress.
FAU - Volpi, Simona
AU  - Volpi S
AD  - Section of Endocrine Physiology, Developmental Endocrinology Branch, National 
      Institute of Child Health and Human Development, NIH, Bethesda, MD 20892-1862, 
      USA.
FAU - Rabadan-Diehl, Cristina
AU  - Rabadan-Diehl C
FAU - Aguilera, Greti
AU  - Aguilera G
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Stress
JT  - Stress (Amsterdam, Netherlands)
JID - 9617529
RN  - 11000-17-2 (Vasopressins)
SB  - IM
MH  - *Adaptation, Physiological
MH  - Animals
MH  - Humans
MH  - Hypothalamo-Hypophyseal System/*physiopathology
MH  - Pituitary-Adrenal System/*physiopathology
MH  - Stress, Physiological/*physiopathology
MH  - Vasopressins/*metabolism
RF  - 60
EDAT- 2004/10/30 09:00
MHDA- 2004/12/16 09:00
CRDT- 2004/10/30 09:00
PHST- 2004/10/30 09:00 [pubmed]
PHST- 2004/12/16 09:00 [medline]
PHST- 2004/10/30 09:00 [entrez]
AID - 4F6YPK0MEHBH22XC [pii]
AID - 10.1080/10253890410001733535 [doi]
PST - ppublish
SO  - Stress. 2004 Jun;7(2):75-83. doi: 10.1080/10253890410001733535.