Evidence map›Paper›PMID 17978601›Full record

ReviewJournal of clinical hypertension (Greenwich, Conn.)2007

Pathophysiology of target-organ disease: does angiotensin II remain the key?

Ronald G Victor

Abstract readReview
In one paragraph

Review in Journal of clinical hypertension (Greenwich, Conn.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Ronald G VictorHypertension Division, Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-8586, USA. ronald.victor@utsouthwestern.edu

Funding

NEURAL MECHANISMS OF CYCLOSPORINE-INDUCED HYPERTENSIONR01HL044010 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI VICTOR, RONALD G · 1990 to 2006
$1.4M
NHLBI NIH HHS R0-1 HL044010
6 · The paper itself

Abstract

Basic research provides an increasingly compelling rationale for renin-angiotensin system (RAS) blockade in hypertension treatment and cardiovascular risk reduction. Clinical trials addressing blood pressure-independent effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, however, have yielded mixed results, in part because of incomplete RAS blockade. Animal studies have shed new light on the complexity of RAS pathways involved in the induction of target-organ damage. New outcomes trials are under way to explore the full potential of more complete RAS blockade with regard to cardiovascular target-organ protection.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsBlood PressureCalcium Channel BlockersCardiovascular DiseasesDisease ProgressionHumansHypertensionLosartanMyocardial InfarctionReninRenin-Angiotensin SystemStrokeTetrazolesAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin II Type 1 Receptor BlockersCalcium Channel BlockersLosartanReninTetrazolesValineValsartan

Identifiers

PMID17978601
PMCPMC8110134

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.