In the presence of 3-isobutyi-l-methylxanthine, VIP produced a dose-related (3 × 10−9 − 10−7 M) increase (g-fold) in cAMP production in isolated HEp-2 cells incubated at 15°C in KRP buffer. Among the peptides structurally related to VIP, including secretin (10−7 M), pancreatic glucagon (10−6 M), PHI, somatostatin-14 (10−6 M), hpGRF (10−8 − 4 × 10−M), GIP (2 × 10−7 M), only PHI (3 × 10−7 M and above) is able to activate the cAMP-generating system in HEp-2 cells, but at 102 times lower potency. Under the same conditions, histamine (10−3 M) was also ineffective, while PGE 2 (10−7 − 10−4 M) increased (0-fold) basal cAMP levels in HEp-2 cells. The VIP effect is related to the interaction os the peptide on VIP recognition sites (12SI-VIP-binding capacity), coupled to the membrane-bound adenylate cyclase. The results indicate that the transformed laryngeal cell line HEp-2 possessesa receptor-cAMP system preferentially activated by VIP (relative potencies: VIP > PHI ≫ other peptides of the secretin family), and suggest that this neuropeptide could modulate biological functions in normal laryngeal epithelia in man.

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