Nitric oxide synthase (NOS) that uses NADPH as a cofactor is an enzyme which produces nitric oxide (NO) from L-arginine. Endothelial-derived (eNOS), inducible (iNOS) and neuronal (nNOS) nitric oxide synthase are 3 known isoforms. | Turk J Biol 25 (2001) 159-169 © TÜB‹TAK Nitric Oxide Synthase in the Skeletal Muscle and Arterioles of Rats with Streptozotosin-Induced Diabetes Mellitus Cihan DEM‹RC‹, Kadriye AKGÜN-DAR, ‹lhan UYANER Department of Biology, Faculty of Science, University of Istanbul, Istanbul - TURKEY Received: Abstract: Nitric oxide synthase (NOS) that uses NADPH as a cofactor is an enzyme which produces nitric oxide (NO) from L-arginine. Endothelial-derived (eNOS), inducible (iNOS) and neuronal (nNOS) nitric oxide synthase are 3 known isoforms. Endothelial NO regulates the vascular tonus and causes the dilatation of vessels, while NOS localized in the sarcolemma of striated muscle plays a role in the regulation of muscle hemodynamics. Many authors have found differences in NO production in some pathological conditions such as diabetes mellitus (DM), hypertension and atherosclerosis. In this study, NADPH-diaphorase (NADPH-d) was histochemically employed to explore any changes in NO production associated with the degree of DM, by detecting the enzyme in the muscle tissue. Diabetes was induced by injecting Swiss albino rats with 65mg/kg of streptozotosin (STZ). Two, 4, 6 and 12 weeks after the STZ injection, the spinotrapezius muscles of the animals were fixed in paraformaldehyde and NADPH-d histochemistry was applied to cryostat sections. Six and 12 weeks after DM, NOS increased both in the muscles and the endothelial cells of arterioles, being more prominent in the 12-week group in which the NADPH-d reaction was also localized in sarcoplasm together with the sarcolemma of muscle fibers than in controls. NOS was more abundant in the 2ndand 3rd-order arterioles in diabetic animals than in controls. After the superfusion of the NW-nitroL-Arginine Methyl Ester (L-NMA) that inhibits NOS, the NADPH-d reaction was still present in 12week DM, while not in controls. ACh superfusion caused endothelial dilation and increased NO production in both the control and diabetic .
