» Articles » PMID: 11872148

Low Molecular Mass Dinitrosyl Nonheme-iron Complexes Up-regulate Noradrenaline Release in the Rat Tail Artery

Overview
Journal BMC Pharmacol
Publisher Biomed Central
Specialty Pharmacology
Date 2002 Mar 2
PMID 11872148
Citations 1
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Dinitrosyl nonheme-iron complexes can appear in cells and tissues overproducing nitric oxide. It is believed that due to their chemical nature these species may be implicated in certain pathophysiological events. We studied the possible role of low molecular mass dinitrosyl iron complexes in the control of noradrenaline release in electrically stimulated rat tail artery.

Results: A model complex, dinitrosyl-iron-thiosulfate (at 1-10 microM) produced a concentration-dependent enhancement of electrical field stimulated [3H]noradrenaline release (up to 2 fold). At the same time, dinitrosyl-iron-thiosulfate inhibited neurogenic vasoconstriction, consistent with its nitric oxide donor properties. A specific inhibitor of cyclic GMP dependent protein kinase, Rp-8pCPT-cGMPS, partially inhibited the effect of dinitrosyl-iron-thiosulfate on neurogenic vasoconstriction, but not on [3H]noradrenaline release. Another model complex, dinitrosyl-iron-cysteine (at 3 microM) elicited similar responses as dinitrosyl-iron-thiosulfate. Conventional NO and NO+ donors such as sodium nitroprusside, S-nitroso-L-cysteine or S-nitroso-glutathione (at 10 microM) had no effect on [3H]noradrenaline release, though they potently decreased electrically-induced vasoconstriction. The "false complex", iron(II)-thiosulfate showed no activity.

Conclusions: Low molecular mass iron dinitrosyl complexes can up-regulate the stimulation-evoked release of vascular [3H]noradrenaline, apparently independently of their NO donor properties. This finding may have important implications in inflammatory tissues.

Citing Articles

Iron nitrosyl complexes as models for biological nitric oxide transfer reagents.

Chiang C, Darensbourg M J Biol Inorg Chem. 2006; 11(3):359-70.

PMID: 16520978 DOI: 10.1007/s00775-006-0084-y.

References
1.
Bergamini S, Rota C, Canali R, STAFFIERI M, Daneri F, Bini A . N-acetylcysteine inhibits in vivo nitric oxide production by inducible nitric oxide synthase. Nitric Oxide. 2001; 5(4):349-60. DOI: 10.1006/niox.2001.0356. View

2.
Rogers P, Ding H . L-cysteine-mediated destabilization of dinitrosyl iron complexes in proteins. J Biol Chem. 2001; 276(33):30980-6. DOI: 10.1074/jbc.M101037200. View

3.
Duffy S, Biegelsen E, Holbrook M, Russell J, Gokce N, Keaney Jr J . Iron chelation improves endothelial function in patients with coronary artery disease. Circulation. 2001; 103(23):2799-804. DOI: 10.1161/01.cir.103.23.2799. View

4.
Ohlmann P, Martinez M, Bucher B, Andriantsitohaina R, Muller B, Schneider F . Effect of lipopolysaccharide treatment on neurogenic contraction and noradrenaline release in rat arteries. Fundam Clin Pharmacol. 2001; 14(6):593-600. DOI: 10.1111/j.1472-8206.2000.tb00445.x. View

5.
Kleschyov A, Muller B, Keravis T, Stoeckel M, STOCLET J . Adventitia-derived nitric oxide in rat aortas exposed to endotoxin: cell origin and functional consequences. Am J Physiol Heart Circ Physiol. 2000; 279(6):H2743-51. DOI: 10.1152/ajpheart.2000.279.6.H2743. View