Publication: Renal effects of cyclooxygenase inhibition when nitric oxide synthesis is reduced and angiotensin II levels are enhanced
Authors
López, Ruth ; Llinás Más, María Teresa ; Salazar, Elena ; Salazar, Francisco Javier
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Publisher
Lippincott, Williams & Wilkins
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DOI
https://doi.org/10.1097/FJC.0000000000000215
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info:eu-repo/semantics/article
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
Abstract
The 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.
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Citation
Journal of Cardiovascular Pharmacology 2015 65:465–472
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