Compensatory mechanisms in myoglobin deficient mice preserve NO homeostasis

Publication date: Available online 4 June 2019Source: Nitric OxideAuthor(s): Ji Won Park, Barbora Piknova, Soumyadeep Dey, Constance T. Noguchi, Alan N. SchechterAbstractThe mechanism for nitric oxide (NO) generation from reduction of nitrate (NO3−) and nitrite (NO2−) has gained increasing attention due to the potential beneficial effects of NO in cardiovascular diseases and exercise performance. We have previously shown in rodents that skeletal muscle is the major nitrate reservoir in the body and that exercise enhances the nitrate reduction pathway in the muscle tissue and have proposed that nitrate in muscle originates from diet, the futile cycle of nitric oxide synthase 1 (NOS1) and/or oxidation of NO by oxymyoglobin. In the present study, we tested the hypothesis that lack of myoglobin expression would decrease nitrate levels in skeletal muscle. We observed a modest but significant decrease of nitrate level in skeletal muscle of myoglobin deficient mice compared to littermate control mice (17.3 vs 12.8 nmol/g). In contrast, a NOS inhibitor, L-NAME or a low nitrite/nitrate diet treatment led to more pronounced decreases of nitrate levels in the skeletal muscle of both control and myoglobin deficient mice. Nitrite levels in the skeletal muscle of both types of mice were similar (0.48 vs 0.42 nmol/g). We also analyzed the expression of several proteins that are closely related to NO metabolism to examine the mechanism by which nitrate and nitrite levels are preserve...
Source: Nitric Oxide - Category: Chemistry Source Type: research