Mechanisms of relaxing response induced by rat/mouse hemokinin-1 in porcine coronary arteries: Roles of potassium ion and nitric oxide
| Autor: | Yuan Long, Cai-Yun Fu, Rui Wang, Min Han, Xiao-Zhu Tian, Juan Chen |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Quinuclidines
medicine.medical_specialty Swine Receptors Prostaglandin Substance P Vasodilation In Vitro Techniques Nitric Oxide Nitroarginine Nitric oxide Mice chemistry.chemical_compound Neurokinin-1 Receptor Antagonists Piperidines Quinoxalines Tachykinins Internal medicine Potassium Channel Blockers medicine Animals Clotrimazole Enzyme Inhibitors Protein Precursors Pharmacology Neurotransmitter Agents Oxadiazoles Dose-Response Relationship Drug biology Tetraethylammonium Potassium channel blocker Receptors Neurokinin-1 Coronary Vessels Potassium channel Rats Nitric oxide synthase Endocrinology Dequalinium chemistry Mechanism of action Anti-Infective Agents Local Potassium biology.protein Endothelium Vascular medicine.symptom medicine.drug |
| Zdroj: | European Journal of Pharmacology. 569:119-125 |
| ISSN: | 0014-2999 |
| DOI: | 10.1016/j.ejphar.2007.04.049 |
| Popis: | Rat and mouse hemokinin-1(r/m hemokinin-1) is a recently described member of the tachykinin family whose cardiovascular functions are not fully understood. In this study, we investigated the mechanisms of the relaxing response induced by r/m hemokinin-1 in isolated porcine coronary arteries by using a specific antagonist of tachykinin NK(1) receptor (SR140333), a nitric oxide synthase inhibitor N(omega)-nitro-L-arginine (L-NNA), and 1H-[1,2,4] Oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), a blocker of cGMP production. r/m Hemokinin-1 (10(-12)-10(-6 )M) evoked a marked endothelium-dependent vasodilatation (E(max)=121.12+/-10.6% and 91.79+/-2.39% in 10(-6) M PGF(2)alpha and 30 mM KCl precontracted arterial rings, respectively) of coronary arteries mediated by activation of endothelial tachykinin NK(1) receptors. Two components contributed to this r/m hemokinin-1-elicited vasodilatation, the first of which was endothelium-derived hyperpolarizing factor (EDHF), which played a major role. This EDHF was identified as a potassium current through certain kinds of potassium channels on the endothelial cell membrane of porcine coronary arteries. Specific antagonists of Ca(2+)-activated K(+) channels (dequalinium and clotrimazole) did not have an inhibitory effect on the r/m hemokinin-1-induced vasodilatation, whereas they did on the substance P-induced vasodilatation. When potassium ion efflux was impaired by a high K(+) concentration (30 mM) or removal of K(+) from the surroundings, NO synthesis was triggered by r/m hemokinin-1 to produce an equivalent EDHF (K(+))-independent vasorelaxation as a compensatory mechanism. |
| Databáze: | OpenAIRE |
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