PMID- 3168920
OWN - NLM
STAT- MEDLINE
DCOM- 19881121
LR  - 20061115
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 123
IP  - 5
DP  - 1988 Nov
TI  - Release of oxytocin and vasopressin by intracerebroventricular vasoactive 
      intestinal polypeptide.
PG  - 2249-54
AB  - Vasoactive intestinal polypeptide (VIP)ergic nerves innervate both the 
      neurohypophysis and the hypothalamus. To test the hypothesis that VIP is a 
      releasing factor for neurohypophyseal hormones, rats were given 
      intracerebroventricular (icv) infusions of VIP in doses varying from 0.3 
      pmol/kg.min to 3 nmol/kg.min for 5 min (0.001-10 micrograms/rat). Serial blood 
      samples were drawn from the vena cava for measurement of oxytocin (OT), 
      vasopressin (AVP), and VIP by RIA. After the VIP infusions mean plasma OT and AVP 
      levels rose in a dose-dependent manner; the rise was significant for both 
      hormones at the dose of 300 pmol/kg.min. Peak levels after infusion of 3 
      nmol/kg.min were greater for OT than AVP [96.1 +/- 14.7 vs. 33.9 +/- 9 microU/ml 
      (mean +/- SE); n = 6]. In addition, the concentration of plasma OT increased more 
      promptly than that of AVP. Plasma OT was significantly raised over control values 
      at 5 min, whereas plasma AVP was not increased until 15 min after the VIP 
      infusion began. The concentration of VIP in peripheral plasma rose somewhat after 
      icv infusions (maximum, 300 pmol/liter 30 min after 10 micrograms/rat), but the 
      rise was only 5% of that observed after systemic infusions of equimolar doses of 
      VIP (maximum, 6000 pmol/liter 5 min after 10 micrograms/rat). Peak plasma OT 
      levels after administration of 3 nmol/kg.min VIP were significantly higher after 
      icv than after systemic infusion of the same dose of VIP reported previously. 
      Intravenous injection of 0.5 ml VIP antiserum with a binding capacity of VIP of 
      2.3 micrograms/ml before the icv administration of VIP (1 microgram/rat) did not 
      prevent the VIP-induced rise in plasma OT and AVP. These observations suggest a 
      central site of action for VIP in OT and AVP release, probably in the 
      hypothalamus. The results are in harmony with the hypothesis that endogenous VIP 
      is a physiological regulator of OT and AVP release in rats.
FAU - Bardrum, B
AU  - Bardrum B
AD  - Institute of Medical Physiology C, Bispebjerg Hospital, Copenhagen, Denmark.
FAU - Ottesen, B
AU  - Ottesen B
FAU - Fahrenkrug, J
AU  - Fahrenkrug J
FAU - Fuchs, A R
AU  - Fuchs AR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 11000-17-2 (Vasopressins)
RN  - 37221-79-7 (Vasoactive Intestinal Peptide)
RN  - 50-56-6 (Oxytocin)
SB  - IM
MH  - Animals
MH  - Cerebral Ventricles/*drug effects
MH  - Dose-Response Relationship, Drug
MH  - Female
MH  - Immunization, Passive
MH  - Kinetics
MH  - Oxytocin/*blood
MH  - Pituitary Gland, Posterior/drug effects/physiology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Vasoactive Intestinal Peptide/administration & dosage/blood/*pharmacology
MH  - Vasopressins/*blood
EDAT- 1988/11/01 00:00
MHDA- 1988/11/01 00:01
CRDT- 1988/11/01 00:00
PHST- 1988/11/01 00:00 [pubmed]
PHST- 1988/11/01 00:01 [medline]
PHST- 1988/11/01 00:00 [entrez]
AID - 10.1210/endo-123-5-2249 [doi]
PST - ppublish
SO  - Endocrinology. 1988 Nov;123(5):2249-54. doi: 10.1210/endo-123-5-2249.