Objective - To study the mechanism by which poly-L-arginine mediates endothelium-dependent relaxation. Methods - Vascular segments with and without endothelium were suspended in organ chambers filled with control solution maintained at 37°C and bubbled with 95% O2/5% CO2. Used drugs: indomethacin, acetycholine, EGTA, glybenclamide, ouabain, poly-L-arginine, methylene blue, NG-nitro-L-arginine, and verapamil and NG-monomethyl-L-arginine. Prostaglandin F2a and potassium chloride were used to contract the vascular rings. Results - Poly-L-arginine (10-11 to 10-7 M) induced concentration-dependent relaxation in coronary artery segments with endothelium. The relaxation to poly-L-arginine was attenuated by ouabain, but was unaffected by glybenclamide. L-NOARG and oxyhemoglobin caused attenuation, but did not abolish this relaxation. Also, the relaxations was unaffected by methylene blue, verapamil, or the presence of a calcium-free bathing medium. The endothelium-dependent to poly-L-arginine relaxation was abolished only in vessels contracted with potassium chloride (40 mM) in the presence of L-NOARG and indomethacin. Conclusion - These experiments indicate that poly-L-arginine induces relaxation independent of nitric oxide.
|Translated title of the contribution||Endothelium-dependent relaxation in response to poly-L-arginine in canine coronary arteries. Implications about hyperpolarization as a mechanism of vasodilatation|
|Number of pages||10|
|Journal||Arquivos brasileiros de cardiologia|
|State||Published - Jun 1 2003|
- Nitric oxide
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine