Effect of passive immunization with antisera to vasoactive intestinal polypeptide and peptide histidine isoleucine amide on 5-hydroxy-L-tryptophan-induced prolactin release in rats.

摘要: The present study was aimed to clarify, by use of the passive immunization method, involvement endogenous vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine amide (PHI)-like peptides in stimulation PRL-like immunoreactive material release induced 5-hydroxy-L-tryptophan (5HTP), a serotonin precursor. We used conscious, freely moving male rats Wistar strain (BW, 250-300 g) chronically cannulated with atrial catheters. Anti-VIP serum (AVS) anti-PHI (APS), each generated rabbits against synthetic porcine VIP natural PHI, respectively, were highly potent [maximum binding capacity (Bmax): AVS, 55.5 nmol/ml; APS, 5.53 nmol/ml] specific. Bolus injection 5HTP (10 mg/kg BW) through catheter caused significant increase plasma PRL (nanograms per ml) pretreated normal rabbit (NRS) [14.3 +/- (SE) 3.8----56.3 11.2], AVS (12.3 3.5----48.5 6.2), APS (10.5 3.9----43.5 8.8), plus (9.0 1.4----28.5 2.7). basal concentrations did not differ significantly among these groups, whereas responses blunted APS-pretreated (P less than 0.05 vs. NRS). To eliminate modification dopaminergic control 5HTP-induced release, next experiment performed repeatedly injected sulpiride, dopamine receptor antagonist (5 BW), every 30 min. first sulpiride prompt marked PRL, followed decreasing but still high levels upon subsequent injections cumulative area after pretreatment or alone lower that NRS 0.05). same dose resulted further exceeding elevated NRS-treated rats. Prior simultaneous administration complete suppression either showed only minimal effect. These results suggest PHI-like are PRL-releasing factors, involved at least mechanism which may be also involved.