ArticleThe Journal of clinical endocrinology and metabolism2012
Nonmodulation as the mechanism for salt sensitivity of blood pressure in individuals with hypertension and type 2 diabetes mellitus.
Article in The Journal of clinical endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 19 citations in OpenAlex.
- Adverse pregnancy outcomes and renal-vascular function in the early years after delivery.American journal of physiology. Heart and circulatory physiology · 2024Article
- Salt restriction lowers blood pressure at rest and during exercise without altering peripheral hemodynamics in hypertensive individuals.American journal of physiology. Heart and circulatory physiology · 2019Article
- Genetics of Human Primary Hypertension: Focus on Hormonal Mechanisms.Endocrine reviews · 2019Review
- Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Review
- Dysregulated aldosterone secretion in persons of African descent with endothelin-1 gene variants.JCI insight · 2017Article
- Age-Related Autonomous Aldosteronism.Circulation · 2017Article
- Renin Phenotypes Characterize Vascular Disease, Autonomous Aldosteronism, and Mineralocorticoid Receptor Activity.The Journal of clinical endocrinology and metabolism · 2017Article
- Salt Restriction in Diabetes.Current diabetes reports · 2015Review
- Effect of low salt diet on insulin resistance in salt-sensitive versus salt-resistant hypertension.Hypertension (Dallas, Tex. : 1979) · 2014Article
- Aldosterone dysregulation with aging predicts renal vascular function and cardiovascular risk.Hypertension (Dallas, Tex. : 1979) · 2014Article
- The influence of sodium- and calcium-regulatory hormone interventions on adipocytokines in obesity and diabetes.Metabolism: clinical and experimental · 2013Article
- Abnormal aldosterone physiology and cardiometabolic risk factors.Hypertension (Dallas, Tex. : 1979) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
contextIt is assumed that in individuals with type 2 diabetes mellitus (T2DM), blood pressure sensitivity to salt intake and the frequency of a low renin state are both increased compared with the nondiabetic population. However, studies supporting these assumptions may have been confounded by participant inclusion criteria, and study results may reflect target organ damage.
objectiveThe objective of this study was to examine in a cohort of T2DM 1) the frequency of salt sensitivity of blood pressure and 2) whether alterations of the renin-angiotensin-aldosterone system (RAAS) contribute to salt sensitivity in this population. DESIGN, PATIENTS, AND
methodsWithin participants of the HyperPATH cohort, four groups were analyzed: 1) T2DM with hypertension (HTN), n=51; 2) T2DM without HTN, n=30; 3) HTN only, n=451; and 4) normotensive, n=209. Phenotype studies were conducted after participants completed two dietary phases: liberal sodium (200 mmol/d) and low sodium (10 mmol/d) for 7 d each. Participants were admitted overnight to a clinical research center after each diet, and supine measurements of the RAAS before and after a 60-min angiotensin II infusion (3 ng/kg·min) were obtained.
resultsMultivariate regression analysis demonstrated that T2DM status (all individuals with T2DM vs. individuals without T2DM) was not associated with the change in mean arterial pressure between the low and liberal sodium diets after accounting for age, gender, body mass index, race, and baseline blood pressure (T2DM status, P=0.5). Furthermore, two intermediate phenotypes of altered RAAS, low renin, and nonmodulation (NMOD), were associated with salt-sensitive blood pressure but occurred at different frequencies in the T2DM-HTN and HTN groups (low renin, 12% T2DM-HTN vs. 29% HTN; NMOD, 41% T2DM-HTN vs. 27% HTN; P=0.01).
conclusionThe frequency of NMOD in participants with T2DM was significantly higher compared with HTN, suggesting that the salt sensitivity often seen in T2DM is driven by NMOD.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.