Abstract
Vasoactive intestinal peptide (VIP) caused concentration-dependent relaxation in precontracted segments of trachea, hilar bronchus, intrapulmonary bronchus and intrapulmonary artery (IPA) isolated from cat lungs. VIP-induced relaxation responses were abolished by preincubation of tissues with the proteolytic enzyme, alpha-chymotrypsin (2 units ml-1). At the concentration employed, alpha-chymotrypsin treatment did not adversely affect tissue viability as isoprenaline and bethanechol continued to relax airways and IPA, respectively. Aprotinin prevented enzymatic degradation of VIP by alpha-chymotrypsin as demonstrated by the ability of VIP to relax tissues incubated with both the peptidase inhibitor and alpha-chymotrypsin. A spectrum of peptidase inhibitors, including aprotinin, leupeptin, bestatin, bacitracin, beta-phenylpropionic acid and captopril, individually or in combination, did not augment the relaxant effects of VIP in isolated pulmonary tissues. These results suggest that local enzymatic degradation may not be a primary route for inactivation of VIP in cat isolated airways and IPA. If VIP acts as a neurotransmitter in these tissues, a mechanism other than enzymatic proteolysis may be responsible for terminating its action.
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