Biosynthesis and Metabolism of Endothelium-Derived Nitric Oxide

Ignarro, Louis J.

doi:10.1146/annurev.pa.30.040190.002535

Cited by 1,234 publications

(448 citation statements)

References 35 publications

Supporting

Mentioning

430

Contrasting

Unclassified

Order By: Relevance

“…Mechanism-Significant inhibitory effects of NOS on platelets and smooth muscle derive from increases in cGMP levels due to activation of soluble guanylyl cyclase (40,41). However, the inhibitory effects of NOS on Fas-induced apoptosis appear to be cGMP-independent: the cell permeable cGMP analog, 8-bromo-cGMP (0.1-1 mM) failed to overcome the effects of L-NMA (Fig.…”

Section: Nos Inhibits Fas-induced Apoptosis Via a Cgmp-independentmentioning

confidence: 99%

Nitric Oxide Inhibits Fas-induced Apoptosis

Mannick¹,

Miao²,

Stamler³

1997

Journal of Biological Chemistry

297

168

View full text Add to dashboard Cite

Section: Nos Inhibits Fas-induced Apoptosis Via a Cgmp-independentmentioning

confidence: 99%

Nitric Oxide Inhibits Fas-induced Apoptosis

Mannick¹,

Miao²,

Stamler³

1997

Journal of Biological Chemistry

297

168

View full text Add to dashboard Cite

“…Nitric oxide (NO) is a critical mediator of a number of biological processes including vasodilation, neurotransmission and host-defense [1][2][3]. Its roles in the cardiovascular system include regulation of vasomotor tone, cell adhesion to the endothelium, inhibition of platelet aggregation, and vascular smooth muscle cell proliferation [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Dose dependent effects of reactive oxygen and nitrogen species on the function of neuronal nitric oxide synthase

Sun

Druhan

Zweíer

2008

Archives of Biochemistry and Biophysics

View full text Add to dashboard Cite

Reactive nitrogen species (RNS) and oxygen species (ROS) have been reported to modulate the function of nitric oxide synthase (NOS); however, the precise dosedependent effects of specific RNS and ROS on NOS function are unknown. Questions remain unanswered regarding whether pathophysiological levels of RNS and ROS alter NOS function, and if this alteration is reversible. We measured the effects of peroxynitrite (ONOO -), superoxide (O 2 .-), hydroxyl radical ( . OH), and H 2 O 2 on nNOS activity. The results showed that NO production was inhibited in a dosedependent manner by all four oxidants, but only O 2 . -and ONOO -were inhibitory at pathophysiological concentrations (≤ 50 μM). Subsequent addition of tetrahydrobiopterin (BH 4 ) fully restored activity after O 2 .-exposure, while BH 4 partially rescued the activity decrease induced by the other three oxidants. Furthermore, treatment with either ONOO -or O 2 .-stimulated nNOS uncoupling with decreased NO and enhanced O 2 .-generation. Thus, nNOS is reversibly uncoupled by O 2 .-(≤ 50 μM), but irreversibly uncoupled and inactivated by ONOO -. Additionally, we observed that the mechanism by which oxidative stress alters nNOS activity involves not only BH 4 oxidation, but also nNOS monomerization as well as possible degradation of the heme.

show abstract

“…⅐ NO is a short-lived intermediate in blood because it is rapidly trapped by the heme iron of hemoglobin and, therefore, one must conclude that nitric oxide uses a transporter to prolong its life-time (3,4). Recently, endogenous S-nitrosothiols have been suggested to be potential ⅐ NO carriers (5,6).…”

mentioning

confidence: 99%