Evidence map›Paper›PMID 16600158›Full record

ReviewCurrent hypertension reports2006

The future of endothelin-receptor antagonism as treatment for systemic hypertension.

Gabriel Vorobiof, Burns C Blaxall, John D Bisognano

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2006. 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
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.

  1. 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

3 authors.

Gabriel VorobiofProgram in Heart Failure and Transplantation, University of Rochester, Cardiology Division, 601 Elmwood Avenue, Box 679T, Rochester, NY 14642-8679, USA.
Burns C Blaxall
John D Bisognano

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelin (ET) is an endogenous peptide secreted predominantly by endothelial cells that mediates its effects via vasoconstriction and hypertrophy of vascular smooth muscle. Because the role of ET has been described in multiple pathologic processes in cardiovascular disease, including hypertension, there has been a strong interest in the development of therapeutic agents that inhibit ET receptors. ET receptor antagonists have shown much promise in disease states such as pulmonary arterial hypertension, essential hypertension, and various forms of secondary hypertension. This review serves to summarize the current role of ET and ET receptor antagonists in both the pathophysiology and the treatment of hypertension.

Indexed as

Endothelin Receptor AntagonistsAntihypertensive AgentsHumansHypertensionTreatment OutcomeVasoconstrictionAntihypertensive AgentsEndothelin Receptor Antagonists

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.