T-kinin has endothelial-dependent vasodilator activity in the
cat.
Santiago, Jos[acute]e A., Hunter C. Champion, and Philip J. Kadowitz.
Department of Pharmacology, Tulane University School of Medicine,
New Orleans, LA 70112
APStracts 3:0432H, 1996.
Responses to T-kinin, a peptide formed from the acute phase substrate
T-kininogen, were investigated in the hindlimb vascular bed of the
cat. Under constant-flow conditions, injections of T-kinin into the
perfusion circuit in doses of 0.03-1 nmol induced rapid dose-related
decreases in perfusion pressure. Responses to T-kinin were similar in
time-course and magnitude to responses to bradykinin and kallidin and
were inhibited by the kinin B2-receptor antagonist, Hoe 140.
Responses to T-kinin were attenuated by an inhibitor of nitric oxide
synthetase and by tetraethylammonium chloride (TEA) and were enhanced
in duration by the cGMP phosphodiesterase inhibitor, Zaprinast.
Responses to T-kinin were not altered by inhibitors of K+ATP
channels, the cyclooxygenase pathway, or by muscarinic or beta
-adrenergic receptor antagonists. These data suggest that vasodilator
responses to T-kinin are mediated by kinin B2-receptor-stimulated
release of nitric oxide form the endothelium and increased smooth
muscle cGMP levels. These results indicate that activation of K+ATP
channels and muscarinic or beta-adrenergic receptors, and the release
of vasodilator prostaglandins are not involved in mediating the
response to T-kinin in the hindlimb circulation of the cat.
Received 17 July 1996; accepted in final form 2 October 1996.
APS Manuscript Number H638-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996