L-arginine dilates cheek pouch arterioles in hamsters with hereditary cardiomyopathy but not in controls.

I. Rubinstein, W. G. Mayhan

Research output: Contribution to journalArticle

20 Scopus citations

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 languageEnglish (US)
Pages (from-to)313-318
Number of pages6
JournalJournal of Laboratory and Clinical Medicine
Volume125
Issue number3
StatePublished - Mar 1 1995

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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