Redox regulation of S-nitrosocysteine-mediated vasodilation in vivo.
This study examined the effects of the lipophobic electron acceptor, nitroblue tetrazolium (2x5 micromol/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]&z. sfnc;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.
Hoque
A
A
Department of Cardiology, University of Louisville, Louisville, KY 40292, USA.
Bates
J N
JN
Lewis
S J
SJ
D000818:Animals; D003545:Cysteine / Q000031:analogs & derivatives* / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D007202:Indicators and Reagents / Q000494:pharmacology*; D008297:Male; D009580:Nitroblue Tetrazolium / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D009603:Nitroso Compounds / Q000494:pharmacology*; D010084:Oxidation-Reduction; D051381:Rats; D017207:Rats, Sprague-Dawley; D026403:S-Nitrosothiols; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*
D007202:Indicators and Reagents; D009603:Nitroso Compounds; D026403:S-Nitrosothiols; D014665:Vasodilator Agents; D009599:Nitroprusside; D009580:Nitroblue Tetrazolium; C021315:S-nitrosocysteine; D003545:Cysteine