Nitric Oxide/cGMP-Independent Vasorelaxation Enhanced by L-Arginine.
- Author:
Seung Ho MOON
1
;
Jong Eun LEE
;
Kwang Jae YOO
;
Bong Suk OH
;
Dong Jun LEE
Author Information
1. Department of Thoracic and Cardiovascular Sugery, Chunnam University, College of Medicine, Korea.
- Publication Type:Original Article
- Keywords:
Vasodilation;
Nitric oxide;
Vasodilator agents;
Aorta
- MeSH:
Animals;
Aorta;
Aorta, Thoracic;
Arginine*;
Endothelium;
Guanosine Monophosphate;
Indomethacin;
Methylene Blue;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Ouabain;
Rats;
Relaxation;
Vasodilation*;
Vasodilator Agents
- From:The Korean Journal of Thoracic and Cardiovascular Surgery
1998;31(2):102-107
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
It has not been clear whether L-arginine plays solely a role contributing to vascular nitric oxide (NO) synthesis. To investigate the mechanisms by which L-arginine induces vasorelaxation, effects of L-arginine on the isometric tension, and tissue NOx and cyclic guanosine monophosphate (cGMP) contents were examined in the isolated rat thoracic aorta. L-Arginine induced a dose-dependent relaxation of aortic rings only with intact endothelium only. The vasorelaxation response to low concentrations of L-arginine was abolished by the pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 10-4 mol/L), whereas the relaxation caused by higher concentrations L-arginine (10-5-10-3 mol/L) was maintained and even more pronounced in the presence of L-NAME. L-Arginine did not affect the vascular tension precontracted with KCl. The vascular tissue contents of NOx/cGMP were not significantly affected by L-arginine, while they were decreased by L-NAME. L-Arginine could not completely recover the NOx/cGMP decreased by L-NAME. Methylene blue only partially antagonized the relaxation response to L-arginine. Indomethacin did not affect the L-arginine-induced vasorelaxation, whereas ouabain markedly attenuated the relaxation. It is suggested that L-arginine induces vasorelaxation not only through its contribution to NO synthesis, but also through enhancing another endothelium-dependent mechanism which is NO/cGMP-independent and cyclooxygenase- independent.
