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Modulation of acute inflammation by endogenous nitric oxide
A Ialenti1, A Ianaro, S Moncada
1Department of Experimental Pharmacology, University of Naples Federico II, Italy.
European Journal of Pharmacology
|February 11, 1992
Summary
Endogenous nitric oxide (NO) plays a key role in acute inflammation, modulating oedema formation. Inhibiting NO synthase reduced inflammation, while L-arginine enhanced it, suggesting NO
Area of Science:
- Pharmacology
- Immunology
- Physiology
Background:
- Acute inflammation involves complex signaling pathways.
- Endogenous nitric oxide (NO) is implicated in inflammatory processes.
- NO synthase (NOS) enzymes are crucial for NO production.
Purpose of the Study:
- To investigate the role of endogenous nitric oxide (NO) in acute inflammation.
- To determine the effects of NO synthase inhibitors and arginine on inflammatory responses.
Main Methods:
- Used NG-nitro-L-arginine methyl ester (L-NAME) and NG-monomethyl-L-arginine (L-NMMA) as NO synthase inhibitors.
- Administered L-arginine and D-arginine to assess their effects.
- Studied carrageenan-induced vascular permeability and paw oedema in rats.
- Examined dextran-induced paw oedema.
- Investigated effects in dexamethasone-treated rats.
Main Results:
- L-NAME and L-NMMA dose-dependently inhibited vascular permeability and oedema.
- L-arginine, but not D-arginine, enhanced inflammatory responses and reversed inhibitor effects.
- L-arginine potentiated dextran-induced oedema and early carrageenan oedema, even with dexamethasone.
Conclusions:
- Endogenous NO is released at acute inflammation sites and modulates oedema.
- NO's role may involve both constitutive and inducible NO synthase, depending on inflammation type and timing.
- Findings highlight NO as a significant mediator in acute inflammatory processes.