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Renal effects of cyclooxygenase inhibition when nitric oxide synthesis is reduced and angiotensin II levels are enhanced

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dc.contributor.authorLópez, Ruth
dc.contributor.authorLlinás Más, María Teresa
dc.contributor.authorSalazar, Elena
dc.contributor.authorSalazar, Francisco Javier
dc.contributor.departmentFisiología
dc.date.accessioned2025-03-17T13:03:47Z
dc.date.available2025-03-17T13:03:47Z
dc.date.issued2015-05
dc.description© 2015 Wolters Kluwer Health, Inc.This document is the Published version of a Published Work that appeared in final form in Journal of Cardiovascular Pharmacology. To access the final edited and published work see https://doi.org/10.1097/FJC.0000000000000215
dc.description.abstractThe involvement of both cyclooxygenase (COX) isoforms in regulating renal function is well known but their interactions with other regulatory mechanisms, such as angiotensin II (Ang II) and nitric oxide (NO), are not well defined. This study has evaluated the relative contribution of both COX isoforms in regulating renal function when NO synthesis is reduced with and without a simultaneous increment in Ang II levels. The renal responses to a nonselective (meclofenamate) or a selective COX2 (nimesulide) inhibitor were examined in dogs pretreated with L-NAME with or without an intrarenal Ang II infusion. Meclofenamate induced a greater (P < 0.05) renal vasoconstriction than nimesulide in dogs pretreated with L-NAME. This vasoconstriction seems to be Ang II-dependent because it was reduced (P < 0.05) by captopril administration. Meclofenamate also induced a greater (P < 0.05) renal vasoconstriction than that elicited by nimesulide in dogs with reduced NO synthesis and elevated Ang II levels. The renal vasoconstriction induced by nimesulide but not that elicited by meclofenamate in dogs pretreated with L-NAME and Ang II, decreased (P < 0.05) during an extracellular volume expansion. These results demonstrate that the nonselective COX inhibition induces a greater renal vasoconstriction than that elicited by the selective COX2 inhibition when NO synthesis is reduced, and when NO synthesis is reduced and Ang II levels are elevated.es
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dc.format.extent8
dc.identifier.citationJournal of Cardiovascular Pharmacology 2015 65:465–472
dc.identifier.doihttps://doi.org/10.1097/FJC.0000000000000215
dc.identifier.issnPrint: 0160-2446
dc.identifier.issnElectronic: 1533-4023
dc.identifier.urihttp://hdl.handle.net/10201/151782
dc.languageenges
dc.publisherLippincott, Williams & Wilkins
dc.relationSin financiación externa a la Universidades
dc.relation.publisherversionhttps://journals.lww.com/cardiovascularpharm/abstract/2015/05000/renal_effects_of_cyclooxygenase_inhibition_when.9.aspx
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectAngiotensin IIes
dc.subjectNitric oxide
dc.subjectCyclooxygenases
dc.subjectRenal blood flow
dc.subjectGlomerular filtration rate
dc.subjectExtracellular volume expansion
dc.titleRenal effects of cyclooxygenase inhibition when nitric oxide synthesis is reduced and angiotensin II levels are enhancedes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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