ArticleJournal of the American Heart Association2017
Collecting Duct Nitric Oxide Synthase 1ß Activation Maintains Sodium Homeostasis During High Sodium Intake Through Suppression of Aldosterone and Renal Angiotensin II Pathways.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- A low dietary sodium dose is associated with a more pronounced aldosterone response in normotensive than in hypertensive individuals.Scientific reports · 2023Pooled it
- Fluid-electrolyte homeostasis requires histone deacetylase function.JCI insight · 2020Pooled it
- Lysine acetylation of aquaporin-3 promotes water permeability but is not essential for urine concentrating ability.American journal of physiology. Renal physiology · 2025Article
- Aryl Hydrocarbon Receptor Activation Promotes Effector CD4+ T Cell Homeostasis and Restrains Salt-Sensitive Hypertension.Function (Oxford, England) · 2025Article
- Endothelial histone deacetylase 1 activity impairs kidney microvascular NO signaling in rats fed a high-salt diet.Acta physiologica (Oxford, England) · 2024Article
- Glycocalyx-Sodium Interaction in Vascular Endothelium.Nutrients · 2023Review
- Role of high-salt diet in non-alcoholic fatty liver disease: a mini-review of the evidence.European journal of clinical nutrition · 2022Review
- Acclimation to a High-Salt Diet Is Sex Dependent.Journal of the American Heart Association · 2022Article
- Hypertension and human immunodeficiency virus: A paradigm for epithelial sodium channels?Frontiers in cardiovascular medicine · 2022Review
- Placental Ischemia Says "NO" to Proper NOS-Mediated Control of Vascular Tone and Blood Pressure in Preeclampsia.International journal of molecular sciences · 2021Review
- Role of collecting duct principal cell NOS1β in sodium and potassium homeostasis.Physiological reports · 2021Article
- 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
- High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021Article
- Sodium-not harmful?Pediatric nephrology (Berlin, Germany) · 2020Article
- Evidence for G-Protein-Coupled Estrogen Receptor as a Pronatriuretic Factor.Journal of the American Heart Association · 2020Article
- Greater natriuretic response to ENaC inhibition in male versus female Sprague-Dawley rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Renal Dopamine Oxidation and Inflammation in High Salt Fed Rats.Journal of the American Heart Association · 2020Article
- Low Nitric Oxide Bioavailability Increases Renin Production in the Collecting Duct.Frontiers in physiology · 2020Article
- The contribution of collecting duct NOS1 to the concentrating mechanisms in male and female mice.American journal of physiology. Renal physiology · 2019Article
- Dynamic changes in histone deacetylases following kidney ischemia-reperfusion injury are critical for promoting proximal tubule proliferation.American journal of physiology. Renal physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundDuring high sodium intake, the renin-angiotensin-aldosterone system is downregulated and nitric oxide signaling is upregulated in order to remain in sodium balance. Recently, we showed that collecting duct nitric oxide synthase 1β is critical for fluid-electrolyte balance and subsequently blood pressure regulation during high sodium feeding. The current study tested the hypothesis that high sodium activation of the collecting duct nitric oxide synthase 1β pathway is critical for maintaining sodium homeostasis and for the downregulation of the renin-angiotensin-aldosterone system-epithelial sodium channel axis. METHODS AND
resultsMale control and collecting duct nitric oxide synthase 1β knockout (CDNOS1KO) mice were placed on low, normal, and high sodium diets for 1 week. In response to the high sodium diet, plasma sodium was significantly increased in control mice and to a significantly greater level in CDNOS1KO mice. CDNOS1KO mice did not suppress plasma aldosterone in response to the high sodium diet, which may be partially explained by increased adrenal
conclusionsThese data demonstrate that high sodium activation of collecting duct nitric oxide synthase 1β signaling induces suppression of systemic and intrarenal renin-angiotensin-aldosterone system, thereby modulating epithelial sodium channel and other sodium transporter abundance and activity to maintain sodium homeostasis.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.