ArticleAmerican journal of physiology. Renal physiology2014
COX-2 mediates angiotensin II-induced (pro)renin receptor expression in the rat renal medulla.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 54 citations in OpenAlex.
- Mutagenesis of the cleavage site of (pro)renin receptor abrogates aldosterone-salt-induced hypertension and renal injury in mice.American journal of physiology. Renal physiology · 2023Article
- The role of (pro)renin receptor and its soluble form in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Collecting duct renin regulates potassium homeostasis in mice.Acta physiologica (Oxford, England) · 2023Article
- Multimodal Blockade of the Renin-Angiotensin System Is Safe and Is a Potential Cancer Treatment for Cats.Veterinary sciences · 2022Article
- Kidney Angiotensin in Cardiovascular Disease: Formation and Drug Targeting.Pharmacological reviews · 2022Review
- NaHypertension (Dallas, Tex. : 1979) · 2022Article
- An update on angiotensin-converting enzyme 2 structure/functions, polymorphism, and duplicitous nature in the pathophysiology of coronavirus disease 2019: Implications for vascular and coagulation disease associated with severe acute respiratory syndrome coronavirus infection.Frontiers in microbiology · 2022Review
- Mutagenesis of the Cleavage Site of Pro Renin Receptor Abrogates Angiotensin II-Induced Hypertension in Mice.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Site-1 Protease-Derived Soluble (Pro)Renin Receptor Contributes to Angiotensin II-Induced Hypertension in Mice.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Aging- and gender-related modulation of RAAS: potential implications in COVID-19 disease.Vascular biology (Bristol, England) · 2021Review
- COX-2-independent activation of renal (pro)renin receptor contributes to DOCA-salt hypertension in rats.American journal of physiology. Renal physiology · 2020Article
- Cell Populations Expressing Stemness-Associated Markers in Vascular Anomalies.Frontiers in surgery · 2020Review
- Sodium butyrate attenuates angiotensin II-induced cardiac hypertrophy by inhibiting COX2/PGE2 pathway via a HDAC5/HDAC6-dependent mechanism.Journal of cellular and molecular medicine · 2019Article
- The (pro)renin receptor in health and disease.Nature reviews. Nephrology · 2019Review
- Review
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- (Pro)renin receptor mediates albumin-induced cellular responses: role of site-1 protease-derived soluble (pro)renin receptor in renal epithelial cells.American journal of physiology. Cell physiology · 2017Article
- Cyclooxygenase 2: protein-protein interactions and posttranslational modifications.Physiological genomics · 2017Review
- Prostaglandin EThe American journal of the medical sciences · 2017Article
- Sodium butyrate suppresses angiotensin II-induced hypertension by inhibition of renal (pro)renin receptor and intrarenal renin-angiotensin system.Journal of hypertension · 2017Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
(Pro)renin receptor (PRR) is predominantly expressed in the distal nephron where it is activated by angiotensin II (ANG II), resulting in increased renin activity in the renal medulla thereby amplifying the de novo generation and action of local ANG II. The goal of the present study was to test the role of cycloxygenase-2 (COX-2) in meditating ANG II-induced PRR expression in the renal medulla in vitro and in vivo. Exposure of primary rat inner medullary collecting duct cells to ANG II induced sequential increases in COX-2 and PRR protein expression. When the cells were pretreated with a COX-2 inhibitor NS-398, ANG II-induced upregulation of PRR protein expression was almost completely abolished, in parallel with the changes in medium active renin content. The inhibitory effect of NS-398 on the PRR expression was reversed by adding exogenous PGE2. A 14-day ANG II infusion elevated renal medullary PRR expression and active and total renin content in parallel with increased urinary renin, all of which were remarkably suppressed by the COX-2 inhibitor celecoxib. In contrast, plasma and renal cortical active and total renin content were suppressed by ANG II treatment, an effect that was unaffected by COX-2 inhibition. Systolic blood pressure was elevated with ANG II infusion, which was attenuated by the COX-2 inhibition. Overall, the results obtained from in vitro and in vivo studies established a crucial role of COX-2 in mediating upregulation of renal medullary PRR expression and renin content during ANG II hypertension.
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