Redox regulation of S-nitrosocysteine-mediated vasodilation in vivo

• Published in: European journal of pharmacology Vol. 408; no. 2; pp. 195 - 198
• Main Authors: Hoque, Azizul, Bates, James N, Lewis, Stephen J
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 17.11.2000; Elsevier
• Subjects: Animals; Biological and medical sciences; Blood vessels and receptors; Cysteine - analogs & derivatives; Cysteine - pharmacology; Fundamental and applied biological sciences. Psychology; Hemodynamics - drug effects; Hemodynamics - physiology; Indicators and Reagents - pharmacology; l- S-Nitrosocysteine; Male; Nitric oxide (NO); Nitroblue Tetrazolium - pharmacology; Nitroprusside - pharmacology; Nitroso Compounds - pharmacology; Oxidation-Reduction; Rat; Rats; Rats, Sprague-Dawley; Redox; S-Nitrosothiols; Vasodilation; Vasodilation - drug effects; Vasodilation - physiology; Vasodilator Agents - pharmacology; Vertebrates: cardiovascular system; Redox; l- S-Nitrosocysteine; Rat; Nitric oxide (NO); Vasodilation; Nitroso compound; Cysteine; Vasodilator agent; Rodentia; Smooth muscle; Biological activity; Endothelium; Muscular relaxation; Vertebrata; Mammalia; Animal; Nitric oxide; Blood vessel; Circulatory system; Redox system
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/S0014-2999(00)00779-2

This study examined the effects of the lipophobic electron acceptor, nitroblue tetrazolium (2×5 μmol/kg, i.v.) on the vasodilation produced by the putative endothelium-derived S-nitrosothiol, l- S-nitrosocysteine (400 nmol/kg, i.v.), and the nitric oxide (NO) donor, ( Z)-1-| N-methyl- N-[6( N-methylammoniohexyl)amino]|diazen-1-ium-1,2-diolate (MAHMA NONOate, 25 nmol/kg, i.v.), in anesthetized rats. The administration of nitroblue tetrazolium resulted in delayed but long-lasting increases in vascular resistances. The l- S-nitrosocysteine-induced vasodilator responses were markedly diminished whereas the MAHMA NONOate-induced responses were not affected by nitroblue tetrazolium. These results support the possibility that l- S-nitrosocysteine interacts with membrane thiols that are subject to nitroblue tetrazolium-induced oxidation (i.e., disulfide-bridge formation) and that nitroblue tetrazolium-induced vasoconstriction may involve a loss of potency of endothelium-derived S-nitrosothiols.