L-Arginine analogues have been widely used to examine the role of endothelium-derived nitric oxide (NO) in vascular responses; however, the effects of the agents on coronary vasomotion are not fully understood. In this study, we examined the effects of the analogues on vasomotion of isolated porcine coronary arteries. Strips of the porcine coronary artery were suspended for isometric tension recording in Krebs-Henseleit solution. L-Arginine analogues, N(ω)-nitro-L-arginine methyl ester (L-NAME, 10-9- 10-3 M), N(G)-monomethyl-L-arginine (L-NMMA, 10-9-10-3 M), and N(G)- nitro-L-arginine (L-NNA, 10-9-10-3 M), caused dose-dependent contractions, which were greater in strips with than in those without endothelium. Those endothelium-dependent contractions were almost abolished by indomethacin (10-5 M) and FeCl2 (10-3 M). The latter reduces prostaglandin H2 to 12-heptadecatrienoic acid, which has no vasoconstrictor effect. These results indicate that the L-arginine analogues cause endothelium-dependent contractions that are mediated by prostaglandin endoperoxides and suggest that they have properties other than simple inhibition of NO synthesis in porcine coronary arteries.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||5 37-5|
|Publication status||Published - 1995|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)