Release of XXXX and vasopressin by intracerebroventricular vasoactive intestinal polypeptide.

@entity35 @entity12180 @entity398
Vasoactive intestinal polypeptide ( @entity12180 )ergic nerves innervate both the neurohypophysis and the hypothalamus. To test the hypothesis that @entity12180 is a releasing factor for neurohypophyseal hormones, @entity35 were given intracerebroventricular (icv) infusions of @entity12180 in doses varying from 0.3 pmol/kg.min to 3 nmol/kg.min for 5 min (0.001-10 micrograms/ @entity35 ). Serial blood samples were drawn from the vena cava for measurement of @entity398 (OT), vasopressin (AVP), and @entity12180 by RIA. After the @entity12180 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 @entity12180 infusion began. The concentration of @entity12180 in peripheral plasma rose somewhat after icv infusions (maximum, 300 pmol/liter 30 min after 10 micrograms/ @entity35 ), but the rise was only 5% of that observed after systemic infusions of equimolar doses of @entity12180 (maximum, 6000 pmol/liter 5 min after 10 micrograms/ @entity35 ). Peak plasma OT levels after administration of 3 nmol/kg.min @entity12180 were significantly higher after icv than after systemic infusion of the same dose of @entity12180 reported previously. Intravenous injection of 0.5 ml @entity12180 antiserum with a binding capacity of @entity12180 of 2.3 micrograms/ml before the icv administration of @entity12180 (1 microgram/ @entity35 ) did not prevent the @entity12180 -induced rise in plasma OT and AVP. These observations suggest a central site of action for @entity12180 in OT and AVP release, probably in the hypothalamus. The results are in harmony with the hypothesis that endogenous @entity12180 is a physiological regulator of OT and AVP release in @entity35 .
