Trial reportBMC nephrology2010
Increased renal sodium absorption by inhibition of prostaglandin synthesis during fasting in healthy man. A possible role of the epithelial sodium channels.
Trial report in BMC nephrology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00281762 (Urinary Aquaporin 2 Excretion After NSAID in Fasting Healthy Human), which is not on this map. Cited by 11 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Urinary Aquaporin 2 Excretion After NSAID in Fasting Healthy Human
Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Effect of vasopressin antagonism on renal handling of sodium and water and central and brachial blood pressure during inhibition of the nitric oxide system in healthy subjects.BMC nephrology · 2014Trial
- Effect of volume expansion with hypertonic- and isotonic saline and isotonic glucose on sodium and water transport in the principal cells in the kidney.BMC nephrology · 2013Trial
- Abnormal increase in urinary aquaporin-2 excretion in response to hypertonic saline in essential hypertension.BMC nephrology · 2012Trial
- Disruption of epithelium integrity by inflammation-associated fibroblasts through prostaglandin signaling.Science advances · 2024Article
- Induction of renal tumor necrosis factor-α and other autacoids and the beneficial effects of hypertonic saline in acute decompensated heart failure.American journal of physiology. Renal physiology · 2021Article
- Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome.PloS one · 2017Article
- The Trafficking of the Water Channel Aquaporin-2 in Renal Principal Cells-a Potential Target for Pharmacological Intervention in Cardiovascular Diseases.Frontiers in pharmacology · 2016Review
- Changes in urinary excretion of water and sodium transporters during amiloride and bendroflumethiazide treatment.World journal of nephrology · 2015Article
- Article
- Aquagenic palmar wrinkling induced by combined use of salazopyrin and indomethacin.Case reports in dermatology · 2013Article
- Primary molecular disorders and secondary biological adaptations in bartter syndrome.International journal of nephrology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTreatment with prostaglandin inhibitors can reduce renal function and impair renal water and sodium excretion. We tested the hypotheses that a reduction in prostaglandin synthesis by ibuprofen treatment during fasting decreased renal water and sodium excretion by increased absorption of water and sodium via the aquaporin2 water channels and the epithelial sodium channels.
methodsThe effect of ibuprofen, 600 mg thrice daily, was measured during fasting in a randomized, placebo-controlled, double-blinded crossover study of 17 healthy humans. The subjects received a standardized diet on day 1, fasted at day 2, and received an IV infusion of 3% NaCl on day 3. The effect variables were urinary excretions of aquaporin2 (u-AQP2), the beta-fraction of the epithelial sodium channel (u-ENaCbeta), cyclic-AMP (u-cAMP), prostaglandin E2 (u-PGE2). Free water clearance (CH2O), fractional excretion of sodium (FENa), and plasma concentrations of vasopressin, angiotensin II, aldosterone, atrial-, and brain natriuretic peptide.
resultsIbuprofen decreased u-AQP2, u-PGE2, and FENa at all parts of the study. During the same time, ibuprofen significantly increased u-ENaCbeta. Ibuprofen did not change the response in p-AVP, u-c-AMP, urinary output, and free water clearance during any of these periods. Atrial-and brain natriuretic peptide were higher.
conclusionDuring inhibition of prostaglandin synthesis, urinary sodium excretion decreased in parallel with an increase in sodium absorption and increase in u-ENaCbeta. U-AQP2 decreased indicating that water transport via AQP2 fell. The vasopressin-c-AMP-axis did not mediate this effect, but it may be a consequence of the changes in the natriuretic peptide system and/or the angiotensin-aldosterone system
trial registrationClinical Trials Identifier: NCT00281762.
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Registered trials
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.