ReviewCurrent opinion in nephrology and hypertension2012
The complex interplay between cyclooxygenase-2 and angiotensin II in regulating kidney function.
Review in Current opinion in nephrology and hypertension, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
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- Review
- Activation of Nrf2 in Mice Causes Early Microvascular Cyclooxygenase-Dependent Oxidative Stress and Enhanced Contractility.Antioxidants (Basel, Switzerland) · 2022Article
- Epidemiology and Pathogenesis of Acute Kidney Injury in the Critically Ill Patients.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2020Review
- Identifying pathophysiological bases of disease in COVID-19.Translational medicine communications · 2020Review
- Iatrogenic hypertension: a bioinformatic analysis.The pharmacogenomics journal · 2019Article
- Fetal Programming of Renal Dysfunction and High Blood Pressure by Chronodisruption.Frontiers in endocrinology · 2019Article
- The Evolving Landscape of Acute Pain Management in the Era of the Opioid Crisis.Current pain and headache reports · 2018Review
- Prostaglandins in the pathogenesis of kidney diseases.Oncotarget · 2018Review
- Enhanced hemodynamic responses to angiotensin II in diabetes are associated with increased expression and activity of AT1 receptors in the afferent arteriole.Physiological genomics · 2017Article
- Association of Nonsteroidal Anti-inflammatory Drug Use With Stroke Among Dialysis Patients.Kidney international reports · 2017Article
- Practical approach to detection and management of acute kidney injury in critically ill patient.Journal of intensive care · 2017Review
- Antioxidant resveratrol restores renal sodium transport regulation in SHR.Physiological reports · 2015Article
- Nonsteroidal anti-inflammatory drugs alter vasa recta diameter via pericytes.American journal of physiology. Renal physiology · 2015Article
- Intrarenal renin-angiotensin system in regulation of glomerular function.Current opinion in nephrology and hypertension · 2014Review
- Impaired ability to modulate glomerular filtration rate in aged female sheep following fetal uninephrectomy.Physiological reports · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewCyclooxygenase-2 (COX-2) plays a critical role in modulating deleterious actions of angiotensin II (Ang II) where there is an inappropriate activation of the renin-angiotensin system (RAS). This review discusses the recent developments regarding the complex interactions by which COX-2 modulates the impact of an activated RAS on kidney function and blood pressure. RECENT
findingsNormal rats with increased COX-2 activity but with different intrarenal Ang II activity because of sodium restriction or chronic treatment with angiotensin-converting enzyme (ACE) inhibitors showed similar renal hemodynamic responses to COX-2-selective inhibition (nimesulide) indicating independence from the intrarenal Ang II activity. COX-2-dependent maintenance of medullary blood flow was consistent and not dependent on dietary salt or ACE inhibition. In contrast, COX-2 influences on sodium excretion were contingent on the prevailing RAS activity. In chronic hypertensive models, COX-2 inhibition elicited similar reductions in kidney function, but COX-2 metabolites contribute to rather than ameliorate the hypertension. SUMMARY: The maintenance of renal hemodynamics reflects direct and opposing effects of Ang II and COX-2 metabolites. The antagonism in water and electrolyte reabsorption is dependent on the prevailing intrarenal Ang II activity. The recent functional experiments demonstrate a beneficial modulation of Ang II by COX-2 except in the presence of inflammation promoted by hypertension, hyperglycemia, and oxidative stress.
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