Key result
l-NAME causes comparable coronary microvessel thickening and fibrosis in wild-type and eNOS-KO mice via NO-independent mechanisms.
Population
Wild-type and endothelial nitric oxide synthase-deficient (eNOS-KO) mice
Comparison
N-nitro-L-arginine methyl ester in drinking… vs Wild-type vs eNOS-KO mice, and treatment with vs…
Design
Preclinical
Follow-up
8 weeks
Authors
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l-NAME induces coronary remodeling via NO-independent pathways in mice; leaves open ACE/oxidative stress targets for human microvascular research.
Long-term vascular effects of l-NAME are not solely mediated by inhibition of endothelial NO synthesis, but involve direct upregulation of local ACE and increased oxidative stress.
Suda et al. (2002) studied Arteriosclerotic Coronary Lesions. N(omega)-nitro-L-arginine methyl ester (l-NAME) vs. Wild-type vs eNOS-KO mice was evaluated on Medial thickening and perivascular fibrosis in coronary microvessels. Long-term treatment with l-NAME caused comparable medial thickening and perivascular fibrosis in coronary microvessels of both wild-type and eNOS-KO mice via NO-independent mechanisms.