AJP - Heart and Circulatory Physiology, Vol 269, Issue 6 2057-H2064, Copyright © 1995 by American Physiological Society
Analysis of responses to kallidin, DABK, and DAK in feline hindlimb vascular bed
J. A. Santiago, E. A. Garrison, H. C. Champion, R. E. Smith, O. Del Rio and P. J. Kadowitz
Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.
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 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 omega-nitro-L-arginine methyl ester (L-NAME) reduced
vasodilator responses to kallidin, DABK, and DAK, whereas meclofenamate,
atropine, and U-37883A, a vascular selective ATP-sensitive K+ (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 or muscarinic
receptors, or the release of vasodilator prostaglandins play little if any
role in mediating responses to kallidin, DABK, or DAK in the hindlimb
vascular bed of the cat.
