Effects of trout bradykinin on the motility of the trout stomach and intestine: evidence for a receptor distinct from mammalian B1 and B2 subtypes

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Abstract
Trout bradykinin ([Arg0,Trp5,Leu8]-bradykinin; trout BK), recently isolated from kallikrein-treated trout plasma, produced sustained and concentration-dependent contractions of isolated longitudinal muscle from rainbow trout stomach (pD2=7.01±0.03) and proximal small intestine (pD2=7.37±0.07). The maximum responses were 85±2% (stomach) and 101±35% (intestine) of the corresponding responses to 10−5 M acetylcholine. Strips of circular smooth muscle from trout stomach and intestine did not contract in response to trout BK. The potency of trout BK on gastric smooth muscle motility was significantly (5 fold; P−5 M) and by 4 fold (P−6 M), but there was no effect on the maximum response. Potency was also significantly reduced in the presence of 10−6 M methysergide (3 fold; P−6 M tetrodotoxin (2 fold, P0,Trp5,Leu8]-BK was a full agonist but was approximately 50 fold less potent (pD2=5.35±0.08) than trout BK, [Arg0,Trp5,Leu8]des-Arg9-BK was a partial agonist (pD2=6.80±0.03; 56±7% of the maximum response to trout BK) but [Trp5,Leu8]-BK, [Trp5,Leu8]-des-Arg9-BK and mammalian BK produced no, or only very weak, contractions of the trout stomach. The mammalian B1 receptor antagonist, [Leu8]des-Arg9-BK was without effect on the response of the trout stomach to trout BK. The potent mammalian B2 receptor antagonist Hoe 140 was a partial agonist (pD2=7.44±0.12; 57±15% of the maximum response to trout BK). We conclude that the effects of trout BK on the motility of rainbow trout gastric smooth muscle are mediated through interaction with a receptor that has appreciably different ligand-binding properties than the mammalian B1 and B2 receptor subtypes. An involvement of arachidonic acid metabolites and 5-hydroxytryptaminergic nerves in the mechanism of action of the peptide is suggested.