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. 1992 Jan 15;281(Pt 2):297–300. doi: 10.1042/bj2810297

Tetrahydrobiopterin-dependent formation of endothelium-derived relaxing factor (nitric oxide) in aortic endothelial cells.

K Schmidt 1, E R Werner 1, B Mayer 1, H Wachter 1, W R Kukovetz 1
PMCID: PMC1130682  PMID: 1297314

Abstract

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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Selected References

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