Distinct Roles of Central and Peripheral Prostaglandin E2 and EP Subtypes in Blood Pressure Regulation

Yang, Tianxin; Du, Yaomin

doi:10.1038/ajh.2012.67

Cited by 40 publications

(37 citation statements)

References 99 publications

(113 reference statements)

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“…COX-2-derived prostanoids include PGE 2 , PGF 2α , PGD 2 , PGI 2 , and thromboxane A 2 with PGE 2 being the dominant one in the kidney [57,58]. Two lines of evidence point to PGE 2 as a major regulator of PRR expression in ICMD cells [9 • ].…”

Section: Role Of Cox-2/ep4 Pathway In Regulation Of Renal Medullary Pmentioning

confidence: 99%

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

Yang

2015

Current Opinion in Pharmacology

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Angiotensin II (AngII) is an octapeptide hormone that plays a central role in regulation of sodium balance, plasma volume, and blood pressure. Its role in the pathogenesis of hypertension is highlighted by the wide use of inhibitors of the renin-angiotensin system (RAS) as the first-line antihypertensive therapy. However, despite intensive investigation, the mechanism of AngII-induced hypertension is still incompletely understood. Although diverse pathways are likely involved, increasing evidence suggests that the activation of intrarenal RAS may represent a dominant mechanism of AngII-induced hypertension. (Pro)renin receptor (PRR), a potential regulator of intrarenal RAS, is expressed in the intercalated cells of the collecting duct (CD) and induced by AngII, in parallel with increased renin in the principal cells of the CD. Activation of PRR elevated PGE2 release and COX-2 expression in renal inner medullary cells whereas COX-2-derived PGE2 via the EP4 receptor mediates the upregulation of PRR during AngII infusion, thus forming a vicious cycle. The mutually stimulatory relationship between PRR and COX-2 in the distal nephron may play an important role in mediating AngII-induced hypertension.

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Section: Role Of Cox-2/ep4 Pathway In Regulation Of Renal Medullary Pmentioning

confidence: 99%

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

Yang

2015

Current Opinion in Pharmacology

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“…COX-1 and COX-2 share 66% homology in amino acid sequence and similar enzymatic properties but represent different cellular expression pattern and regulation (7–9). COX-1 is constitutively expressed in most tissues, whereas COX-2 shows low expression under baseline and it is induced in response to cytokines and other physiological or pathological stimuli (2).…”

Section: Introductionmentioning

confidence: 99%

“…This nephron segment is also the primary target site for PGE 2 to regulate sodium transport (11–13). In general, renal medullary PGE 2 functions a natriuretic factor that inhibits sodium reabsorption and causes vasodilation, thus eliciting natriuresis (9). Renal medullary PGE 2 synthesis is also elevated after high salt loading (14).…”

Section: Introductionmentioning

confidence: 99%

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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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“…For instance, in mouse kidney, low-dose PGE 2 vasoconstricts through EP1 and EP3 receptors but at a higher dose vasodilates through activation of EP2 and EP4 (50). Similarly, PGs administered centrally and systemically exert differing effects dependent on the receptor types involved (51). Alternatively Indo may exert differential effects depending on the physiological state of the tissue.…”

Section: Discussionmentioning

confidence: 99%

Peripheral Corticotropin-Releasing Factor Receptor Type 2 Activation Increases Colonic Blood Flow Through Nitric Oxide Pathway in Rats

2015

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Background Corticotropin-releasing factor (CRF) peptides exert profound effects on the secretomotor function of the gastrointestinal tract. Nevertheless, despite the presence of CRF peptides and receptors in colonic tissue, their influence on colonic blood flow (CBF) is unknown. Aim To determine the effect and mechanism of members of the CRF peptide family on CBF in isoflurane-anesthetized rats. Methods Proximal CBF was measured with laser Doppler flowmetry simultaneously with mean arterial blood pressure (MABP) measurement. Rats were injected with intravenous human/rat CRF (CRF1>CRF2 affinity), mouse urocortin 2 (mUcn2, selective CRF2 agonist) or sauvagine (SVG, CRF2>CRF1 affinity) at 1 – 30 μg/kg. The nitric oxide (NO) synthase inhibitor, L-NAME (3 mg/kg, iv), the cyclooxygenase inhibitor, indomethacin (Indo, 5 mg/kg, ip) or selective CRF2 antagonist, astressin2-B (Ast2B, 50 μg/kg, iv) was given before SVG injection (10 μg/kg, iv). Results SVG and mUcn2 dose-dependently increased CBF while decreasing MABP and colonic vascular resistance (CVR). CRF had no effect on CBF, but increased CVR. The hyperemic effect of SVG was inhibited by L-NAME but not by Indo, whereas hypotension was partially reduced by L-NAME. Sensory denervation had no effect on SVG-induced changes. Ast2B inhibited SVG-induced hyperemia and decreased CVR, and partially reduced the hypotension. Conclusions Peripheral CRF2 activation induces colonic hyperemia through NO synthesis, without involving prostaglandin synthesis or sensory nerve activation, suggesting a direct action on the endothelium and myenteric neurons. Members of the CRF peptide family may protect the colonic mucosal via the activation of the CRF2 receptor.

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Distinct Roles of Central and Peripheral Prostaglandin E2 and EP Subtypes in Blood Pressure Regulation

Cited by 40 publications

References 99 publications

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

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

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

Peripheral Corticotropin-Releasing Factor Receptor Type 2 Activation Increases Colonic Blood Flow Through Nitric Oxide Pathway in Rats

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