Evidence map›Paper›PMID 25374825›Full record

ReviewWorld journal of nephrology2014

Regulatory roles of nitric oxide and angiotensin II on renal tubular transport.

Shoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Renal sodium handling and sodium sensitivity.Kidney research and clinical practice · 2017
    Review
  6. Kidney tubules: intertubular, vascular, and glomerular cross-talk.Current opinion in nephrology and hypertension · 2016
    Review
  7. Article
  8. 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

7 authors at 1 institution in 1 country.

Shoko HoritaShoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki, Department of Internal Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Motonobu NakamuraShoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki, Department of Internal Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Ayumi ShiraiShoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki, Department of Internal Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Osamu YamazakiShoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki, Department of Internal Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Nobuhiko SatohShoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki, Department of Internal Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Masashi SuzukiShoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki, Department of Internal Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
George SekiShoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki, Department of Internal Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Suzuki (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin II (AngII) and nitric oxide (NO). AngIIcan significantly raise blood pressure via effects on the heart, vasculature, and renal tubules. AngII generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules. Stimulation of renal proximal tubule (PT) transport is thought to be essential for AngII-mediated hypertension. However, AngII has a biphasic effect on in vitro PT transport in mice, rats, and rabbits: stimulation at low concentrations and inhibition at high concentrations. On the other hand, NO is generally thought to inhibit renal tubular transport. In PTs, NO seems to be involved in the inhibitory effect of AngII. A recent study reports a surprising finding: AngII has a monophasic stimulatory effect on human PT transport. Detailed analysis of signalling mechanisms indicates that in contrast to other species, the human NO/guanosine 3',5'-cyclic monophosphate/extracellular signal-regulated kinase pathway seems to mediate this effect of Ang II on PT transport. In this review we will discuss recent progress in understanding the effects of AngII and NO on renal tubular transport.

Indexed as

Angiotensin IIDistal tubulesNa+ transportNitric oxideProximal tubulesThick ascending limb

Identifiers

PMID25374825
PMCPMC4220364
OpenAlexW2053312545

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.