| 19038273 |
Chen GP, Ye Y, Li L, Yang Y, Qian AB, Hu SJ: Endothelium-independent vasorelaxant effect of sodium ferulate on rat thoracic aorta. Life Sci. 2009 Jan 16;84(3-4):81-8. Epub 2008 Nov 14.
AIMS: This study was designed to investigate the effects of sodium ferulate (SF) on rat isolated thoracic aortas and the possible mechanisms. MAIN METHODS: Isometric tension was recorded in response to drugs in organ bath. Cytosolic free Ca (2+) concentration ([Ca (2+)](i)) was measured using Fluo-3 in cultured rat aortic smooth muscle cells (RASMC). KEY FINDINGS: SF (0.1-30 mM) relaxed the isolated aortic rings precontracted with phenylephrine (PE) and high-K (+) in a concentration-dependent manner with respective pD (2) of 2.7+/-0.02 and 2.6+/-0.06. Mechanical removal of endothelium did not significantly modify the SF-induced relaxation. In Ca (2+)-free solution, SF noticeably inhibited extracellular Ca (2+)-induced contraction in high-K (+) and PE pre-challenged rings, and suppressed the transient contraction induced by PE and caffeine. The vasorelaxant effect of SF was unaffected by various K (+) channel blockers such as tetraethylammonium, glibenclamide, 4-aminopyridine, and barium chloride. In addition, SF concentration-dependently reduced the contraction induced by phorbol-12-myristate-13-acetate, an activator of protein kinase C (PKC), in the absence of extracellular Ca (2+), with the pD (2) of 2.9+/-0.03. In RASMC, SF had no effect on PE- or KCl-induced [Ca (2+)](i) increase either in the presence or in the absence of external Ca (2+). SIGNIFICANCE: These results indicate that SF acts directly as a non-selective relaxant to vascular smooth muscle. The direct inhibition of the common pathway after [Ca (2+)](i) increase may account for the SF-induced relaxation in Ca (2+)-dependent contraction, while the blockage of the PKC-mediated contractile mechanism is likely responsible for the SF-induced relaxation in Ca (2+)-independent contraction. |
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