The purpose of this study was to determine whether suffusion of L-arginine alone induces vasodilation in the cheek pouch of hamsters with hereditary cardiomyopathy in comparison with controls, and whether these effects are mediated by the L-arginine/nitric oxide biosynthetic pathway. Using intravital microscopy, we found that suffusion of L-arginine for 20 minutes induced a significant, stereospecific concentration-dependent vasodilation in hamsters with hereditary cardiomyopathy but not in controls (p < 0.05). These responses were abrogated by suffusion of the nitric synthase inhibitor NG-L-arginine methyl ester (L-NAME) but not by suffusion of D-NAME. Suffusion of nitroglycerin, a nitric oxide donor, induced significant vasodilation of similar magnitude in both groups (p < 0.05). L-NAME had no significant effects on nitroglycerin-induced responses in both groups. We conclude that direct application of L-arginine alone to the peripheral microcirculation in cardiomyopathy induces significant vasodilation that is mediated, most likely, via a nitric oxide-dependent mechanisms(s). We suggest that a reversible, L-arginine-responsive impairment in the constitutive L-arginine/nitric oxide biosynthetic pathway is present in the peripheral microcirculation in cardiomyopathy.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Laboratory and Clinical Medicine|
|State||Published - Mar 1 1995|
ASJC Scopus subject areas
- Pathology and Forensic Medicine