[Effect of emodin on NO-cGMP signal pathway in rat vascular endothelium in vitro].
OBJECTIVE
To investigate the vasorelaxation effect of emodin and its relationship with NO-cGMP signal pathway.


METHODS
Changes of tension of rat thoracic aortic rings were measured by MedLab biologic signal collection system, and the activity of total nitric oxide synthase (tNOS), constitutive NOS (cNOS) and inducible NOS (iNOS) in endothelium after being treated with emodin was determined with nitric acid reductase method.


RESULTS
Emodin relaxed the phenylephrine and potasium chlorate induced contraction of aortic rings, either with or without intact endothelium, in a concentration-dependent manner. Pretreatment of no-specific potassium channel blocker strontium chloride (CsCL) could attenuate the vasorelaxation effect of emodin on aortic rings without intact endothelium, but it could not inhibit vasorelaxation of emodin on aortic rings with intact endothelium. This vasorelaxation action of emodin (40 micromol/L) could be partial blocked by NOS inhibitor L-NAME and guanylate cyclase inhibitor ODQ, with the vasorelaxation range dropped to 64.76 +/- 13.73% and 6.28 +/- 4.79% respectively. Moreover, emodin (40 micromol/L) increased iNOS activity significantly.


CONCLUSIONS
The concentration-dependent vasorelaxation effect of emodin might act by activating the NO-cGMP pathway in vascular endothelium.
Wang
Wei-min
WM
Department of Basic Theory, Medical College, Zhejiang University, Hangzhou.
Yu
Yan-qin
YQ
Qian
Ling-bo
LB
D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology; D006152:Cyclic GMP / Q000378:metabolism*; D004642:Emodin / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000378:metabolism*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D014665:Vasodilator Agents / Q000494:pharmacology*
D014665:Vasodilator Agents; D009569:Nitric Oxide; D006152:Cyclic GMP; D004642:Emodin