الفهرس 
INTRODUCTION AND AIM OF THE WORKOnly 14 pages are availabe for public view
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Abstract
Recent evidences point to an important role of NO in regulation of skeletal muscle contraction and modulation of glucose transport. So this study aims to investigate the role of NO on skeletal muscle contraction and glucose uptake by skeletal muscle in diabetic and denervateed rats. The work was divided into 2 parts : to study glucose uptake and muscle contraction. Each part was divided 3 main groups. Each main Each main group was divided into 3 subgroups, each includes 8 experiment, to study the effect of NO donor (SNP), NO precursor (L<U+00AC>arginine), NO synthase blocker (LNAMI) on skeletal muscle glucose uptake as well as muscle contraction. Consequently it can be concluded that: Nitric oxide promotes glucose uptake and inhibits skeletal muscle contraction, and these effects act to preserve energy stores. * Modulation of NO pathway by NO donors in skeletal muscle could provide a novel approach to increase glucose transport in diabetic and denervated skeletal muscle. The direct inhibitory effect of NO donor on skeletal muscle contraction appears to act as a ?brake? perhaps to protect the muscle from fatigue or mechanical damage. The depressing effect of NO on skeletal muscle contraction in diabetic and denervated muscle can be prevented by potentiation of the indirect action of NO on the muscle NO/cGMP pathway. Both exogenous NO and_ NO synthase Mockers dampens the force of skeletal muscle contraction. This means that endogenous NO is essential for optimal skeletal muscle contraction.