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강윤환,양인준,Kathleen G. Morgan,신흥묵 생화학분자생물학회 2012 Experimental and molecular medicine Vol.44 No.12
Cinnamyl alcohol (CAL) is known as an antipyretic, and a recent study showed its vasodilatory activity without explaining the mechanism. Here we demonstrate the vasodilatory effect and the mechanism of action of CAL in rat thoracic aorta. The change of tension in aortic strips treated with CAL was measured in an organ bath system. In addition, vascular strips or human umbilical vein endothelial cells (HUVECs) were used for biochemical experiments such as Western blot and nitrite and cyclic guanosine monophosphate (cGMP)measurements. CAL attenuated the vasoconstriction of phenylephrine (PE, 1 μM)-precontracted aortic strips in an endothelium-dependent manner. CAL-induced vasorelaxation was inhibited by pretreatment with NG-nitro-L-arginine methyl ester (L-NAME; 10-4 M),methylene blue (MB; 10-5 M) and 1 H-[1,2,4]-oxadiazolole-[4,3-a] quinoxalin-10one, (ODQ; 10-6 or 10-7M) in the endothelium-intact aortic strips. Atrial natriuretic peptide (ANP; 10-8 or 10-9 M) did not affect the vasodilatory effect of CAL. The phosphorylation of endothelial nitric oxide synthase (eNOS) and generation of nitric oxide (NO) were stimulated by CAL treatment in HUVECs and inhibited by treatment with L-NAME. In addition,cGMP and PKG1 activation in aortic strips treated with CAL were also significantly inhibited by L-NAME. Furthermore, CAL relaxed Rho-kinase activator calpeptin-precontracted aortic strips, and the vasodilatory effect of CAL was inhibited by the ATP-sensitive K+ channel inhibitor glibenclamide (Gli; 10-5 M) and the voltage-dependent K+ channel inhibitor 4-aminopyridine (4-AP; 2 × 10-4 M). These results suggest that CAL induces vasorelaxation by activating K+ channels via the NO-cGMP-PKG pathway and the inhibition of Rho-kinase.
Enhanced Stretch-Induced Myogenic Tone in the Basilar Artery of Spontaneously Hypertensive Rats
Ahn, Duck-Sun,Choi, Soo-Kyoung,Kim, Young-Hwan,Cho, Young-Eun,Shin, Heung Mook,Morgan, Kathleen G.,Lee, Young-Ho S. Karger 2007 Journal of vascular research Vol.44 No.3
<P>We investigated if the magnitude of myogenic tone in the basilar artery of SHR differs from that in WKY and, if so, whether RhoA- or PKC-dependent mechanisms were involved. Myogenic tone was developed in response to stretch. Stretch-induced myogenic contraction was significantly greater in the SHR than WKY in the presence of external Ca<SUP>2+</SUP>. However, in the absence of external Ca<SUP>2+</SUP>, stretch did not evoke a myogenic tone. The [Ca<SUP>2+</SUP>]<SUB>i</SUB>-induced contraction was larger in SHR than WKY and the [Ca<SUP>2+</SUP>]<SUB>i</SUB>-force curve was significantly shifted to the left in SHR compared to WKY. Y-27632 significantly inhibited stretch-induced myogenic tone, but the inhibitory effect was larger in the SHR than WKY. However, PKC inhibitors had no significant effect on the myogenic tone. RhoA and PKCε were expressed at higher levels in the SHR compared to the WKY. RhoA and PKCα translocated from the cytosol to the cell membrane in response to stretch in both animals, but PKCε was translocated only in SHR. Our results strongly suggest that stretch-induced myogenic tone is enhanced in SHR, and the activation of RhoA/Rho kinase plays an important role in the enhanced myogenic tone in SHR.</P><P>Copyright © 2007 S. Karger AG, Basel</P>