Tetrahydrobiopterin-dependent formation of endothelium-derived relaxing factor (nitric oxide) in aortic endothelial cells
K Schmidt, ER Werner, B Mayer, H Wachter… - Biochemical …, 1992 - portlandpress.com
K Schmidt, ER Werner, B Mayer, H Wachter, WR Kukovetz
Biochemical Journal, 1992•portlandpress.comInhibition of tetrahydrobiopterin (H4biopterin) biosynthesis in endothelial cells almost
completely abolished the agonist-induced formation of endothelium-derived relaxing factor
(EDRF)(NO). This inhibitory effect could be antagonized when H4biopterin biosynthesis was
restored by activating a salvage pathway. These data indicate that the formation of EDRF
strictly depends on the presence of intracellular H4biopterin, which, in addition to Ca2+, may
represent a further physiological and/or pathophysiological regulatory of endothelial NO …
completely abolished the agonist-induced formation of endothelium-derived relaxing factor
(EDRF)(NO). This inhibitory effect could be antagonized when H4biopterin biosynthesis was
restored by activating a salvage pathway. These data indicate that the formation of EDRF
strictly depends on the presence of intracellular H4biopterin, which, in addition to Ca2+, may
represent a further physiological and/or pathophysiological regulatory of endothelial NO …
Inhibition of tetrahydrobiopterin (H4biopterin) biosynthesis in endothelial cells almost completely abolished the agonist-induced formation of endothelium-derived relaxing factor (EDRF) (NO). This inhibitory effect could be antagonized when H4biopterin biosynthesis was restored by activating a salvage pathway. These data indicate that the formation of EDRF strictly depends on the presence of intracellular H4biopterin, which, in addition to Ca2+, may represent a further physiological and/or pathophysiological regulatory of endothelial NO synthases.
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