Evidence map›Paper›PMID 17384992›Full record

ReviewClinical and experimental nephrology2007

Regulatory mechanism of "K+recycling" for Na +reabsorption in renal tubules.

Masayuki Tanemoto

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and experimental nephrology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 88% of its field
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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. Role and mechanisms of regulation of the basolateral KActa physiologica (Oxford, England) · 2017
    Review
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

1 author at 1 institution in 1 country.

Masayuki TanemotoDivision of Nephrology, Hypertension and Endocrinology, Department of Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai, 980-8574, Japan. mtanemoto-tky@umin.ac.jp
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension is one of the predominant risk factors for the progression of renal impairment, and the most common disorder in industrialized societies. Because reduction of the systemic blood pressure in hypertension can halt the progression of renal impairment, it is imperative to appropriately control the systemic blood pressure. Recent genetic analysis has reconfirmed that renal maladjustment of Na(+)-homeostasis, which determines the extracellular fluid volume, is a key element in the pathogenesis of hypertension. The distal tubules adjust the net Na(+)-excretion according to Na(+)-ingestion and maintain the Na(+)-homeostasis. The distal convoluted tubules and the connecting tubules are the predominant sites for the adjustment in individuals with a modern lifestyle. In these tubules, Na(+)-reabsorption depends on "K(+)-recycling", which is conducted through K(+) channels. Because the functional expression of K(+) channels in these tubules is regulated by signal motifs for intracellular localization, the adjustment of "K(+)-recycling" through the modification of signal motifs could be a new target for the treatment of hypertension.

Indexed as

Blood PressureHomeostasisHumansHypertensionKidney TubulesPotassiumSodiumPotassiumSodium

Identifiers

PMID17384992
OpenAlexW2081907528

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.