Cinnamyl alcohol attenuates vasoconstriction by activation of K+ channels via NO-cGMP-protein kinase G pathway and inhibition of Rho-kinase

Experimental and Molecular Medicine

Volumn 44, Issue 12, 2012, Pages 749-755

  Kang, Yun Hwan ^a   Yang, In Jun ^a   Morgan, Kathleen G ^b   Shin, Heung Mook ^a  

^a Dongguk University   (South Korea)

^b BOSTON UNIVERSITY   (United States)

Author keywords

Cinnamyl alcohol; Cyclic GMP dependent protein kinase type I; Nitric oxide; Potassium channels; Rho associated kinases

Indexed keywords

1H 1,2,4 OXADIAZOLO[4,3 A]QUINOXALIN 1 ONE; 4 AMINOPYRIDINE; ATRIAL NATRIURETIC FACTOR; CALPEPTIN; CINNAMYL ALCOHOL; CYCLIC GMP DEPENDENT PROTEIN KINASE; ENDOTHELIAL NITRIC OXIDE SYNTHASE; GLIBENCLAMIDE; METHYLENE BLUE; N(G) NITROARGININE METHYL ESTER; NITRIC OXIDE; PHENYLEPHRINE; POTASSIUM CHANNEL; RHO KINASE;

ANIMAL TISSUE; ARTICLE; ATTENUATION; CELL VIABILITY; CONCENTRATION RESPONSE; CONTROLLED STUDY; CYTOTOXICITY TEST; DRUG EFFECT; DRUG MECHANISM; DRUG STRUCTURE; ENZYME ACTIVATION; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; HUMAN; HUMAN CELL; MALE; NONHUMAN; RAT; SIGNAL TRANSDUCTION; THORACIC AORTA; UMBILICAL VEIN ENDOTHELIAL CELL; VASOCONSTRICTION; VASODILATATION; WESTERN BLOTTING;

EID: 84871352491     PISSN: 12263613     EISSN: 20926413     Source Type: Journal    
DOI: 10.3858/emm.2012.44.12.083     Document Type: Article

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