Evidence map›Paper›PMID 28676941›Full record

ReviewCurrent hypertension reports2017

Molecular Mechanisms of Sodium-Sensitive Hypertension in the Metabolic Syndrome.

Jonathan M Nizar, Vivek Bhalla

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Marine drugs · 2018
    Trial
  2. Article
  3. Article
  4. Maternal High-Fat Diet and Offspring Hypertension.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Insights from direct renal insulin infusion: a new hammer for an age-old nail.American journal of physiology. Renal physiology · 2018
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Jonathan M NizarDivision of Nephrology, Department of Medicine, Stanford University School of Medicine, 777 Welch Rd, Suite DE, Palo Alto, CA, 94305, USA.
Vivek BhallaDivision of Nephrology, Department of Medicine, Stanford University School of Medicine, 777 Welch Rd, Suite DE, Palo Alto, CA, 94305, USA. vbhalla@stanford.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewWe review the known mechanisms of sodium-sensitive hypertension in the metabolic syndrome with a focus on preclinical models, differences between these models, and methodological limitations. We also identify future directions for a better understanding and treatment of this common condition. RECENT

findingsRigorous methodologies to measure blood pressure in preclinical models may clarify some of the inconsistencies in the literature. Renal, neural, hormonal, and cardiovascular systems are dysregulated and contribute to elevated blood pressure. Local renin-angiotensin systems enhance systemic hormone signaling to increase blood pressure. Since the original description of metabolic syndrome, investigators from many fields have contributed to an increasingly complex and mechanistic understanding of this common condition. These systems integrate to regulate sodium transport in the kidney leading to hypertension and enhanced sodium sensitivity. An array of non-uniform preclinical models are used and support clinical studies to inform which models are pathophysiologically relevant for further mechanistic studies to guide targeted therapy.

Indexed as

Renin-Angiotensin SystemAnimalsBlood PressureDiet, High-FatHumansHypertensionInflammationInsulin ResistanceKidneyMetabolic SyndromeObesityOxidative StressSodiumSodium, DietarySympathetic Nervous SystemSodiumSodium, DietaryHigh fat dietInsulin resistanceMineralocorticoid receptorObesitySodium sensitivity

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.