Abstract
Tolerance to nitroglycerin through proteasomal degradation of aldehyde dehydrogenase-2 in a genetic mouse model of ascorbate deficiency
Highlights
L-Gulonolactone oxidase-deficient mice (Gulo(−/−)) were used to study the effects of ascorbate deficiency on aortic relaxation and lowering of blood pressure by nitroglycerin (GTN)
Tolerance to nitroglycerin through proteasomal degradation of aldehyde dehydrogenase-2 in a genetic mouse model of ascorbate deficiency
Special emphasis was given to changes in expression and activity of vascular aldehyde dehydrogenase-2 (ALDH2), which has been recently characterized as key enzyme of vascular GTN bioactivation
Summary
L-Gulonolactone oxidase-deficient mice (Gulo(−/−)) were used to study the effects of ascorbate deficiency on aortic relaxation and lowering of blood pressure by nitroglycerin (GTN). Special emphasis was given to changes in expression and activity of vascular aldehyde dehydrogenase-2 (ALDH2), which has been recently characterized as key enzyme of vascular GTN bioactivation
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