ANALYSIS OF RESPONSES TO KALLIDIN, DABK, AND DAK IN FELINE HINDLIMB VASCULAR BED

Responses to kallidin, des-Arg(9)-bradykinin (DABK), and des-Arg(10)-k allidin (DAK) were investigated in the hindlimb vascular bed of the ca t under constant-flow conditions. Injections of kallidin, DABK, and DA K into the hindlimb perfusion circuit produced dose-dependent vasodila tor responses in the hindlimb vascular bed. Vasodilator responses to k allidin and bradykinin (BK) were similar in magnitude and time course, and both peptides were similar to 100-fold more potent than DABK or D AK. Responses to kallidin were decreased by the kinin B-2 antagonist, HOE 140, whereas responses to DABK and DAK were reduced by des-Arg(9)[ Leu(8)]BK, a kinin B-1-receptor antagonist. N-omega-nitro-L-arginine m ethyl ester (L-NAME) reduced vasodilator responses to kallidin, DARK, and DAK, whereas meclofenamate, atropine, and U-37883A, a vascular sel ective ATP-sensitive K+ (K-ATP(+)) channel-blocking agent, did not alt er responses to the three peptides. These data suggest that both kinin B-1 and B-2 receptors are normally present in the hindlimb vascular b ed. These data also suggest that kinin B-1 and B-2 receptor-mediated v asodilator responses are mediated by the release of nitric oxide and t hat the activation of K-ATP(+) channels or muscarinic receptors, or th e release of vasodilator prostaglandins play little if any role in med iating responses to kallidin, DABK, or DAK in the hindlimb vascular be d of the cat.