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  • Title: Endothelium-dependent and -independent vasorelaxation induced by CIJ-3-2F, a novel benzyl-furoquinoline with antiarrhythmic action, in rat aorta.
    Author: Chang GJ, Lin TP, Ko YS, Lin MS.
    Journal: Life Sci; 2010 Jun 05; 86(23-24):869-79. PubMed ID: 20388521.
    Abstract:
    AIMS: This study was designed to examine the mechanism of relaxation induced by CIJ-3-2F, a benzyl-furoquinoline antiarrhythmic agent, in rat thoracic aorta at the tissue and cellular levels. MAIN METHODS: Isometric tension of rat aortic ring was measured in response to drugs. Ionic channel activities in freshly dissociated aortic vascular smooth muscle cells (VSMCs) were investigated using a whole-cell patch-clamp technique. KEY FINDINGS: CIJ-3-2F relaxed both phenylephrine (PE) and high KCl (60mM)-induced contractions with respective pEC(50) (-log EC(50)) values of 6.91+/-0.07 and 6.32+/-0.06. Removal of endothelium or pretreatment with nitric oxide (NO)-pathway inhibitors N(omega)-nitro-l-arginine methyl ester (L-NAME), N(G)-monomethyl-l-arginine (L-NMMA), N(5)-(1-iminoethyl)-l-ornithine (L-NIO), hemoglobin, methylene blue or 1H-[1,2,4]oxadiazolo[4,2-alpha]quinoxalin-1-one (ODQ) reduced the relaxant effect of CIJ-3-2F. Relaxation to CIJ-3-2F was also attenuated by K(+) channel blockers tetraethylammonium (TEA) or 4-aminopyridine (4-AP), but not by charybdotoxin plus apamin, iberiotoxin, glibenclamide, or BaCl(2). CIJ-3-2F non-competitively antagonized the contractions induced by PE, Ca(2+), and Bay K8644 in endothelium-denuded rings. In addition, CIJ-3-2F inhibited both the phasic and tonic contractions induced by PE but did not affect the transient contraction induced by caffeine. CIJ-3-2F reduced the Ba(2+) inward current through L-type Ca(2+) channel (IC(50)=4.1microM) and enhanced the voltage-dependent K(+) (K(v)) current in aortic VSMCs. SIGNIFICANCE: These results suggest that CIJ-3-2F induced both endothelium-dependent and -independent vasorelaxation; the former is likely mediated by the NO/cGMP pathway whereas the latter is probably mediated through inhibition of Ca(2+) influx or inositol 1,4,5-triphosphate (IP(3))-sensitive intracellular Ca(2+) release, or through activation of K(v) channels.
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