Evidence map›Paper›PMID 18367029›Full record

ReviewCurrent hypertension reports2008

Endothelin-1 and hypertension: from bench to bedside.

Donald E Kohan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. O-GlcNAcylation: a novel pathway contributing to the effects of endothelin in the vasculature.American journal of physiology. Regulatory, integrative and comparative physiology · 2011
    Review
  9. 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

1 author at 1 institution in 1 country.

Donald E KohanDivision of Nephrology, University of Utah Health Sciences Center, 1900 East 30 North, Salt Lake City, UT 84132, USA. donald.kohan@hsc.utah.edu
University of Utah · US

Funding

NIDDK NIH HHS DK96392
6 · The paper itself

Abstract

Endothelin-1 (ET-1) exerts a wide range of biologic effects that can influence systemic blood pressure. Recent studies indicate that increased activity of the ET system in the vasculature, with resultant activation of primarily ET A receptors, can contribute to hypertension. In contrast, decreased production of ET-1 in the renal medulla, and reduced activation of collecting duct ET B receptors, can also elevate systemic blood pressure. Both ET A and combined A/B receptor blockers reduce blood pressure in hypertensive patients. Several important questions remain with respect to the ET system in hypertension, including how ET receptor antagonists will interact with other antihypertensive agents, which receptor subtypes should be targeted, and what the effect of ET blockade will be on hypertension-related end-organ damage as opposed to blood pressure alone.

Indexed as

Blood PressureEndothelin-1EndothelinsHumansHypertensionReceptor, Endothelin AReceptor, Endothelin BEndothelin-1EndothelinsReceptor, Endothelin AReceptor, Endothelin B

Identifiers

PMID18367029
OpenAlexW2156858470

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.