Analysis of responses to kallidin, dabk, and dak in the feline
hindlimb vascular bed.
Santiago, Jos[acute]e A., Etoi A. Garrison, Hunter C. Champion,
Raelanda E. Smith, Oscar Del Rio, and Philip J. Kadowitz.
Department of Pharmacology, Tulane University School of Medicine,
New Orleans, LA 70112
APStracts 2:0240H, 1995.
Responses to kallidin, des-Arg9-bradykinin (DABK), and des-Arg10
-kallidin (DAK) were investigated in the hindlimb vascular bed of the
cat under constant flow conditions. Injections of kallidin, DABK, and
DAK into the hindlimb perfusion circuit produced dose-dependent
vasodilator responses in the hindlimb vascular bed. Vasodilator
responses to kallidin and bradykinin (BK) were similar in magnitude
and in time-course, and both peptides were approximately 100-fold
more potent than DABK or DAK. Responses to kallidin were decreased by
the kinin B2 antagonist, Hoe 140; whereas responses to DABK and DAK
were reduced by des-Arg9[Leu8]-BK, a kinin B1 receptor antagonist.
N_-Nitro-L-arginine methyl ester (L-NAME) reduced vasodilator
responses to kallidin, DABK, and DAK; whereas meclofenamate,
atropine, and U37883A, a vascular selective K+ATP channel blocking
agent, did not alter responses to the three peptides. These data
suggest that both kinin B1 and B2 receptors are normally present in
the hindlimb vascular bed. These data also suggest that kinin B1 and
B2 receptor-mediated vasodilator responses are mediated by the
release of nitric oxide, and that the activation of K+ATP channels,
muscarinic receptors, or the release of vasodilator prostaglandins
plays little if any role in mediating responses to kallidin, DABK, or
DAK in the hindlimb vascular bed of the cat.
Received 19 December 1994; accepted in final form 31 May 1995.
APS Manuscript Number H1113-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.