Ja. Santiago et al., T-KININ HAS ENDOTHELIUM-DEPENDENT VASODILATOR ACTIVITY IN THE CAT, American journal of physiology. Heart and circulatory physiology, 41(3), 1997, pp. 1491-1498
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 perfu
sion circuit in doses of 0.03-1 nmol induced rapid dose-related decrea
ses in perfusion pressure. Responses to T-kinin were similar in time c
ourse and magnitude to responses to bradykinin and kallidin and were i
nhibited by the kinin B-2-receptor antagonist, Hoe-140. Responses to T
-kinin were attenuated by an inhibitor of nitric oxide synthase and by
tetraethylammonium chloride and were enhanced in dura by the guanosin
e 3',5'-cyclic monophosphate (cGMP) phosphodiesterase inhibitor zaprin
ast. Responses to T-kinin were not altered by inhibitors of K-ATP(+) c
hannels, by the cyclooxygenase pathway, or by muscarinic or beta-adren
ergic-receptor antagonists. These data suggest that vasodilator respon
ses to T-kinin are mediated by kinin B-2-receptor-stimulated release o
f nitric oxide from the endothelium and increased smooth muscle cGMP l
evels. These results indicate that activation of K-ATP(+) channels and
muscarinic or beta-adrenergic receptors and the release of vasodilato
r prostaglandins are not involved in mediating the response to T-kinin
in the hindlimb circulation of the cat.