Tetrahydrobiopterin induces vasodilation via enhancement of cGMP level.
Studies with cell homogenates and cultures had indicated earlier that nitric oxide (NO) synthase is dependent on tetrahydrobiopterin, which apparently functions as a cofactor for the enzyme. The present results showed a vasodilator response to tetrahydrobiopterin in precontracted aorta, which is attained via an increase of the intracellular cyclic GMP level. Furthermore, L-Ng-nitro-arginine-methyl ester inhibits the tetrahydrobiopterin-induced vasodilation, showing the involvement of NO synthase.
Van Amsterdam
J G
JG
National Institute of Public Health and Environmental Protection, Bilthoven, Netherlands.
Wemer
J
J
D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001708:Biopterins / Q000031:analogs & derivatives* / Q000494:pharmacology; D006152:Cyclic GMP / Q000378:metabolism*; D066298:In Vitro Techniques; D008729:Methoxamine / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D019331:NG-Nitroarginine Methyl Ester; D011863:Radioimmunoassay; D051381:Rats; D014664:Vasodilation / Q000187:drug effects*
D001708:Biopterins; D001120:Arginine; C003402:sapropterin; D006152:Cyclic GMP; D008729:Methoxamine; D019331:NG-Nitroarginine Methyl Ester