| Title | Characterization of bradykinin-induced endothelium-independent contraction in equine basilar artery. | | Author(s) | Ueno D, Yabuki A, Obi T, Shiraishi M, Nishio A, Miyamoto A | | Institution | Department of Veterinary Pharmacology, Faculty of Agriculture, Kagoshima University, Kagoshima, Japan. | | Source | J Vet Pharmacol Ther 2009 Jun; 32(3):264-70. | | Abstract | We investigated the effect of bradykinin (BK) on isolated equine basilar arterial rings with and without endothelium. BK induced concentration-dependent contraction of resting arterial rings and no relaxation when the rings were precontracted by prostaglandin F(2alpha). The maximal response and pD(2) value were 161.2 +/- 28.1% (to 60 mm KCl-induced contraction) and 8.24 +/- 0.25 respectively. The cumulative concentration-response curve for BK was not shifted to the right by des-Arg(9)-[Leu(8)]-BK (a B(1)-receptor antagonist), HOE140 (a B(2)-receptor antagonist) or NPC567 (another B(2)-receptor antagonist). In four of six basilar arteries, NPC567 induced concentration-dependent contraction. Indomethacin (a cyclooxygenase inhibitor), nordihydroguaiaretic acid (a lipoxygenase inhibitor), quinacrine (a phospholipase A(2) inhibitor), tetrodotoxin (a selective blocker of Na(+) channels), guanethidine (a nor-adrenergic neuron blocking drug), phentolamine (an alpha-adrenoceptor antagonist), Nomega-nitro-l-arginine (l-NNA, a nitric oxide (NO) synthase inhibitor) and endothelial denudation did not affect the BK-induced contraction. l-NNA and indomethacin induced contraction and relaxation under resting vascular tone respectively. These results suggest that endothelial cells are not involved in BK-induced contraction and that the contraction is not mediated via activation of known B(1) and B(2) receptors. Arachidonic acid metabolites and neurotransmitters like norepinephrine and NO might not play a role in BK-induced contraction in equine basilar artery. | | Language | eng | | Pub Type(s) | Journal Article
| | PubMed ID | 19646091 |
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