Abstract
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) |
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Pages (from-to) | 313-318 |
Number of pages | 6 |
Journal | Journal of Laboratory and Clinical Medicine |
Volume | 125 |
Issue number | 3 |
State | Published - Mar 1995 |
Externally published | Yes |
ASJC Scopus subject areas
- Pathology and Forensic Medicine