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Cited by 306

The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.

Endogenous nitric oxide enhances prostaglandin production in a model of renal inflammation.

Open access
Salvemini, D, Seibert, K, Masferrer, J L, Misko, T P, Currie, M G, Needleman, P·1994·Journal of Clinical Investigation

Abstract

The interaction between nitric oxide (NO) and cyclooxygenase (COX) was studied in a rabbit model of renal inflammation, the ureteral obstructed hydronephrotic kidney (HNK). Ex vivo perfusion of the HNK but not the control kidney (e.g., unobstructed contralateral kidney, CLK), led to a time-dependent release of nitrite (NO2-), a breakdown product of NO. Stimulation of the HNK with bradykinin (BK) evoked a time-dependent increase in prostaglandin E2 (PGE2) production. NG-monomethyl-L-arginine (L-NMMA), which blocks the activity of both constitutive and inducible nitric oxide synthase (cNOS and iNOS), aminoguanidine, a recently described selective iNOS inhibitor, dexamethasone, or cycloheximide abolished the release of NO2- and attenuated the exaggerated BK-induced PGE2 production. This supports the existence of iNOS and COX-2 in the HNK. In the CLK, BK elicited release of both NO2- and PGE2 but this did not augment with time. L-NMMA but not aminoguanidine, dexamethasone, or cycloheximide attenuated NO2- and PGE2 release indicative of the presence of constitutive but not inducible NOS or COX. The current study suggests that the endogenous release of NO from cNOS in the CLK activates a constitutive COX resulting in optimal PGE2 release by BK. In addition, in the HNK, NO release from iNOS activates the induced COX resulting in markedly increased release of proinflammatory prostaglandin. The broader implication of this study is that the cyclooxygenase isozymes are potential receptor targets for nitric oxide.

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Metadata

Authors
Salvemini, D., Seibert, K., Masferrer, J. L., Misko, T. P., Currie, M. G., & Needleman, P.
Venue
Journal of Clinical Investigation
Published
1994-05-01
Volume
93
Issue
5
Pages
1940-1947
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2018789478
Cited by
306
References
33
FWCI
20.61
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Endogenous nitric oxide enhances prostaglandin production in a model of renal inflammation. https://app.cochat.ai/papers/10.1172/jci117185
The paper
Salvemini, D., Seibert, K., Masferrer, J. L., Misko, T. P., Currie, M. G., & Needleman, P. (1994). Endogenous nitric oxide enhances prostaglandin production in a model of renal inflammation. Journal of Clinical Investigation. https://doi.org/10.1172/jci117185

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.