PMID- 11268412
OWN - NLM
STAT- MEDLINE
DCOM- 20010419
LR  - 20220321
IS  - 0077-8923 (Print)
IS  - 0077-8923 (Linking)
VI  - 917
DP  - 2000
TI  - Perturbations of arginine vasopressin secretion during inflammatory stress. 
      Pathophysiologic implications.
PG  - 825-34
AB  - Pro-inflammatory cytokines, such as interleukin-1 beta (IL-1 beta), interleukin-6 
      (IL-6), and tumor necrosis factor-alpha (TNF alpha), released from inflammatory 
      foci, can activate the hypothalamus to produce corticotrophin-releasing hormone 
      (CRH) and arginine vasopressin (AVP). These hypothalamic peptides in synergy 
      increase ACTH production by the pituitary gland and hence corticosteroid (CS) 
      secretion by the adrenal cortices. CS dampens inflammation. The pituitary also 
      produces prolactin (PRL), which is pro-inflammatory, and macrophage inhibitory 
      factor (MIF), which by counteracting the anti-inflammatory and immunosuppressive 
      effects of CS, is pro-inflammatory. Lewis rats develop a variety of 
      induced-autoimmune inflammatory conditions, such as streptococcal cell wall 
      arthritis, whereas the histocompatible F344 Fisher rats are resistant to this 
      condition. Lewis rats have a defective hypothalamic-pituitary adrenal (HPA) 
      response to a variety of hypothalamic stimuli, but have augmented systemic 
      secretion of AVP. Patients with rheumatoid arthritis (RA) have deficient CS with 
      exaggerated PRL responses to inflammatory stimuli. Within inflammatory foci, CRH 
      is pro-inflammatory. AVP, which augments autologous mixed lymphocyte reactions, 
      can replace the IL-2 requirement for gamma IFN production by T cells via V1a 
      receptors, and potentiates primary antibody responses, is also pro-inflammatory. 
      Lewis rats have significantly high plasma levels, hypothalamic content, and in 
      vitro release of AVP in comparison to the inflammatory disease-resistant Fischer 
      rats. Immunoneutralization of AVP attenuates inflammatory responses. In 
      Sprague-Dawley rats, AVP potentiates PRL secretion. Preliminary studies in 
      patients with RA have shown that the circulating levels of AVP are significantly 
      increased, which might be a compensatory response to low CS levels or a result of 
      elevated levels of IL-6 in these patients but could nevertheless contribute to 
      rheumatoid inflammation. A similar observation has been made in patients with 
      ankylosing spondylitis.
FAU - Chikanza, I C
AU  - Chikanza IC
AD  - Bone & Joint Research Unit, St. Bartholomews & Royal London School of Medicine 
      and Dentistry, New Science Building, Charterhouse Square, London EC1 6BQ, UK. 
      i.c.chikanza@mds.qmw.ac.uk
FAU - Petrou, P
AU  - Petrou P
FAU - Chrousos, G
AU  - Chrousos G
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 113-79-1 (Arginine Vasopressin)
SB  - IM
MH  - Animals
MH  - Arginine Vasopressin/*immunology
MH  - Humans
MH  - Inflammation/immunology
MH  - *Neuroimmunomodulation
MH  - Stress, Physiological/*immunology/physiopathology
RF  - 89
EDAT- 2001/03/28 10:00
MHDA- 2001/04/21 10:01
CRDT- 2001/03/28 10:00
PHST- 2001/03/28 10:00 [pubmed]
PHST- 2001/04/21 10:01 [medline]
PHST- 2001/03/28 10:00 [entrez]
AID - 10.1111/j.1749-6632.2000.tb05448.x [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2000;917:825-34. doi: 10.1111/j.1749-6632.2000.tb05448.x.