Release of Oxytocin and Vasopressin by Intracerebroventricular Vasoactive Intestinal Polypeptide*

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Abstract
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 intracerebroventicular (icv) infusions of VIP in doses varying from 0.3 pmol/kg .cntdot. min to 3 nmol/kg .cntdot. min for 5 min (.001-10 .mu.g/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 .cntdot. min. Peak levels after infusion of 3 nmol/kg .cntdot. min were greater for OT than AVP [96.1 .+-. 14.7 vs. 33.9 .+-. 9 .mu.U/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 .mu.g/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 .mu.g/rat). Peak plasma OT levels after administration of 3 nmol/kg .cntdot. 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 .mu.g/ml before the icv administration of VIP (1 .mu.g/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.