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Published on: October 26, 2020
The complex interplay between cyclooxygenase-2 and angiotensin II in regulating kidney function.
Torrance Green1, Alexis A Gonzalez, Kenneth D Mitchell
1Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana 70112, USA.
Cyclooxygenase-2 (COX-2) modulates angiotensin II (Ang II) effects on kidney function. While COX-2 benefits renal hemodynamics, its role in electrolyte balance depends on the renin-angiotensin system (RAS) activity.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Inflammation Research
Background:
- Cyclooxygenase-2 (COX-2) is crucial in counteracting detrimental angiotensin II (Ang II) effects during renin-angiotensin system (RAS) overactivation.
- Understanding the interplay between COX-2 and RAS is vital for managing kidney function and blood pressure.
Purpose of the Study:
- To review recent advancements on how COX-2 modulates the impact of an activated RAS on renal hemodynamics and blood pressure.
- To elucidate the complex interactions between COX-2 and the RAS in the context of kidney function.
Main Methods:
- Review of recent functional experiments and findings.
- Analysis of studies involving COX-2 selective inhibition (nimesulide) in normal rats with varying intrarenal Ang II activity.
- Examination of data from chronic hypertensive models.
Main Results:
- COX-2 inhibition's effect on renal hemodynamics was independent of intrarenal Ang II activity in normal rats.
- COX-2 maintains medullary blood flow irrespective of dietary salt or ACE inhibition.
- COX-2's influence on sodium excretion is dependent on RAS activity.
- In hypertensive models, COX-2 inhibition reduced kidney function, and its metabolites exacerbated hypertension.
Conclusions:
- Renal hemodynamics are influenced by opposing Ang II and COX-2 metabolite effects.
- Water and electrolyte reabsorption antagonism by COX-2 is contingent on intrarenal Ang II activity.
- COX-2 beneficially modulates Ang II, except during inflammation associated with hypertension, hyperglycemia, and oxidative stress.
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