Crosstalk between (Pro)renin receptor and COX-2 in the renal medulla during angiotensin II-induced hypertension

Yang, Tianxin

doi:10.1016/j.coph.2014.12.011

Cited by 26 publications

(20 citation statements)

References 63 publications

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“…Also, our results found that the inhibition of AngII and COX2 blocked RIIH-induced PRR expression, which confirmed the essential roles of AngII and COX2 in increasing renal PRR expression during RIIH. Previous studies documented that COX2/PGE2/EP4 pathway is responsible for high PRR expression in the renal medulla during AngII-induced hypertension (Green et al 2012, Wang et al 2014, Yang 2015. However, in the current study, RIIH induced AngII which might activate the COX2/PGE2/EP4 pathway and lead to an increase in expression of PRR in the kidney.…”

Section: Discussioncontrasting

confidence: 47%

Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

Alanazi¹,

Uddin²,

Fakhruddin

et al. 2017

IJM

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Background: Recurrent insulin-induced hypoglycemia (RIIH) is an avoidable consequence in the therapeutic management of diabetes mellitus. RIIH has been implicated in causing hypertension through an increase in renal and systemic AngII production. Objective: The present study was performed to assess the hypothesis that chronic insulin treatment enhances AngII and COX2 formation which in turn increases (pro) renin receptor (PRR) expression and NADPH oxidase-mediated oxidative stress, leading to renal and cardiac injury. Methods:The present studies were conducted in Male Sprague Dawley rats treated with daily subcutaneous injections of 7u/kg insulin or saline for 14 days. On the 14th day, surgery was performed for treatment infusion (captopril 12mg/kg, NS398 0.3mg/kg or vehicle), and renal interstitial fluid sample and urine collections for biomarker measurements. At the end of the experiments, kidneys and hearts were harvested to evaluate PRR and NOX2 (NADPH oxidase subunit) expression and oxidative stress. Results: We found that RIIH enhanced AngII and COX2 activity, leading to renal PRR expression and NADPH oxidase-induced oxidative stress in the heart and kidney. 8-isoprostane was evaluated as a renal biomarker of oxidative stress, which was induced in insulin treated animals and modulated by captopril and NS398. In addition, there was a slight increase in NGAL, a urinary biomarker of acute kidney injury (AKI), in insulin treated animals when compared to control. Conclusion: These results demonstrate that RIIH induces renal PRR expression and oxidative stress through increasing AngII and COX2 in the heart and kidney, leading to end-organ damage.

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Section: Discussioncontrasting

confidence: 47%

Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

Alanazi¹,

Uddin²,

Fakhruddin

et al. 2017

IJM

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“…In vitro and in vivo results suggested a crucial role of COX-2 in mediating upregulation of renal medullary (pro)renin receptor (PRR) expression and rennin content during ANG II-induced hypertension. (18, 61). Our subsequent study further claimed that the specific COX-2/PGE 2 /EP 4 pathway mediated the upregulation of renal medullary PRR expression by ANGII, leading to activation of intrarenal RAS and enhancement of the hypertensive response (62).…”

Section: Discussionmentioning

confidence: 99%

“…The goal of this review to summarize the major findings in the literature concerning the regulation and function of renal medullary COX-2 during high salt loading. For general knowledge about renal PG pathway, you are referred to a number of previous review articles (9, 16–18). …”

Section: Introductionmentioning

confidence: 99%

Regulation and function of renal medullary cyclooxygenase-2 during high salt loading

Yang

Liu

2017

Front Biosci

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Prostaglandins (PGs) are important autocrine/paracrine regulators that contribute to sodium balance and blood pressure control. Along the nephron, the highest amount of PGE2 is found in the distal nephron, an important site for fine-tuning of urinary sodium and water excretion. Cylooxygenase-2 (COX-2) is abundantly expressed in the renal medulla and its expression along with urinary PGE2 excretion is highly induced by chronic salt loading. Factors involved in high salt-induced COX-2 expression in the renal medulla include the hypertonicity, fluid shear stress (FSS), and hypoxia-inducible factor-1α (HIF-1 α). Site-specific inhibition of COX-2 in the renal medulla of Sprague-Dawley rats causes sodium retention and salt-sensitive hypertension. Together, these results support the concept that renal medullary COX-2 functions an important natriuretic mediator that is activated by salt loading and its products promote sodium excretion and contribute to maintenance of sodium balance and blood pressure.

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“…Li, et al, 2015), and a cyclooxygenase (COX)-2–dependent pathway in the kidney (Wang, et al, 2014). Increased PRR expression may further promote the production of Ang II, ultimately resulting in positive feedback regulation of the receptor itself and the development of hypertension (Wang, et al, 2014; T. Yang, 2015).…”

Section: Introductionmentioning

confidence: 99%

The critical role of the central nervous system (pro)renin receptor in regulating systemic blood pressure

Jensen

Peng

et al. 2016

Pharmacology & Therapeutics

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The systemic renin–angiotensin system (RAS) has long been recognized as a critically important system in blood pressure (BP) regulation. However, extensive evidence has shown that a majority of RAS components are also present in many tissues and play indispensable roles in BP regulation. Here, we review evidence that RAS components, notably including the newly identified (pro)renin receptor (PRR), are present in the brain and are essential for the central regulation of BP. Binding of the PRR to its ligand, prorenin or renin, increases BP and promotes progression of cardiovascular diseases in an angiotensin II-dependent and -independent manner, establishing the PRR a promising antihypertensive drug target. We also review the existing PRR blockers, including handle region peptide and PRO20, and propose a rationale for blocking prorenin/PRR activation as a therapeutic approach that does not affect the actions of the PRR in vacuolar H+-ATPase and development. Finally, we summarize categories of currently available antihypertensive drugs and consider future perspectives.

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Crosstalk between (Pro)renin receptor and COX-2 in the renal medulla during angiotensin II-induced hypertension

Cited by 26 publications

References 63 publications

Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

Regulation and function of renal medullary cyclooxygenase-2 during high salt loading

The critical role of the central nervous system (pro)renin receptor in regulating systemic blood pressure

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