ArticleCirculation research2010
Cyclooxygenase-2-dependent prostacyclin formation and blood pressure homeostasis: targeted exchange of cyclooxygenase isoforms in mice.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 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
21 citing papers in PubMed, 48 citations in OpenAlex.
- Cyclooxygenase-1 deletion in 5 × FAD mice protects against microglia-induced neuroinflammation and mitigates cognitive impairment.Translational neurodegeneration · 2025Article
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Potential beneficial effects of long-term aspirin use on the prevalence of colorectal cancer: a population-based study of the US Nationwide Inpatient Sample.Cancer causes & control : CCC · 2024Article
- Selenocoxib-3, a novel anti-inflammatory therapeutic effectively resolves colitis.Molecular and cellular biochemistry · 2023Article
- The Effects of Pain and Analgesic Medications on Blood Pressure.Current hypertension reports · 2022Review
- NaHypertension (Dallas, Tex. : 1979) · 2022Article
- Cyclooxygenase-2 Modulates Glycosaminoglycan Production in the Skin During Salt Overload.Frontiers in physiology · 2020Article
- Differential compensation of two cyclooxygenases in renal homeostasis is independent of prostaglandin-synthetic capacity under basal conditions.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Genomic and lipidomic analyses differentiate the compensatory roles of two COX isoforms during systemic inflammation in mice.Journal of lipid research · 2018Article
- Flipping the cyclooxygenase (Journal of lipid research · 2018Article
- Clinical Pharmacology and Cardiovascular Safety of Naproxen.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2017Review
- Regulation and function of renal medullary cyclooxygenase-2 during high salt loading.Frontiers in bioscience (Landmark edition) · 2017Review
- Inhibition of the Prostaglandin Transporter PGT Lowers Blood Pressure in Hypertensive Rats and Mice.PloS one · 2015Article
- Cyclooxygenase-2-derived prostaglandin E₂ promotes injury-induced vascular neointimal hyperplasia through the E-prostanoid 3 receptor.Circulation research · 2013Article
- Major urinary metabolites of 6-keto-prostaglandin F2α in mice.Journal of lipid research · 2013Article
- Biased suppression of TP homodimerization and signaling through disruption of a TM GxxxGxxxL helical interaction motif.Journal of lipid research · 2013Article
- An eicosanoid-centric view of atherothrombotic risk factors.Cellular and molecular life sciences : CMLS · 2012Review
- Vascular COX-2 modulates blood pressure and thrombosis in mice.Science translational medicine · 2012Article
- PharmGKB summary: very important pharmacogene information for PTGS2.Pharmacogenetics and genomics · 2011Article
- Extracellular cAMP-adenosine pathways in the mouse kidney.American journal of physiology. Renal physiology · 2011Article
Corrections and comments
- Erratum issuedSymth, Emer M [corrected to Smyth, Emer M]
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
rationaleCyclooxygenase (COX)-derived prostanoids (PGs) are involved in blood pressure homeostasis. Both traditional nonsteroidal antiinflammatory drugs (NSAIDs) that inhibit COX-1 and COX-2 and NSAIDs designed to be selective for inhibition of COX-2 cause sodium retention and elevate blood pressure.
objectiveTo elucidate the role of COX-2 in blood pressure homeostasis using COX-1>COX-2 mice, in which the COX-1 expression is controlled by COX-2 regulatory elements. METHODS AND
resultsCOX-1>COX-2 mice developed systolic hypertension relative to wild types (WTs) on a high-salt diet (HSD); this was attenuated by a PGI(2) receptor agonist. HSD increased expression of COX-2 in WT mice and of COX-1 in COX-1>COX-2 mice in the inner renal medulla. The HSD augmented in all strains urinary prostanoid metabolite excretion, with the exception of the major PGI(2) metabolite that was suppressed on regular chow and unaltered by the HSD in both mutants. Furthermore, inner renal medullary expression of the receptor for PGI(2), but not for other prostanoids, was depressed by HSD in WT and even more so in both mutant strains. Increasing osmolarity augmented expression of COX-2 in WT renal medullary interstitial cells and again the increase in formation of PGI(2) observed in WTs was suppressed in cells derived from both mutants. Intramedullary infusion of the PGI(2) receptor agonist increased urine volume and sodium excretion in mice.
conclusionsThese studies suggest that dysregulated expression of the COX-2 dependent, PGI(2) biosynthesis/response pathway in the renal inner renal medulla undermines the homeostatic response to a HSD. Inhibition of this pathway may contribute directly to the hypertensive response to NSAIDs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.