Evidence map›Paper›PMID 20962112›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Renal denervation modulates angiotensin receptor expression in the renal cortex of rabbits with chronic heart failure.

Sarah C Clayton, Karla K V Haack, Irving H Zucker

Registry-linked trialAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01870310 (Long Term Study on the Possible Beneficial Effects of Catheterised Renal Denervation in Patients With Heart Failure and Left Ventricular Systolic Dysfunction Who Are Already on Standard Medical Therapy.), which is not on this map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.6field-weighted citation impact, top 7% 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.

NCT01870310 naunknown statusnot on this mapstarted 2012, after this paper: background citation

Long Term Study on the Possible Beneficial Effects of Catheterised Renal Denervation in Patients With Heart Failure and Left Ventricular Systolic Dysfunction Who Are Already on Standard Medical Therapy.

TypeinterventionalSponsorUniversity Hospital OlomoucRan2012 to 2016Enrolled50ConditionsHeart FailureArmsCatheterised renal denervation
3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The denervation or activation of renal sympathetic nerve and renal blood flow.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2023
    Review
  6. N-type calcium channel and renal injury.International urology and nephrology · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Vascular control of kidney epithelial transporters.American journal of physiology. Renal physiology · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Renal sympathetic nerve activation via αKidney research and clinical practice · 2019
    Article
  17. Article
  18. Article
  19. Review
  20. 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 at 1 institution in 1 country.

Sarah C ClaytonDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA.
Karla K V Haack
Irving H Zucker
University of Nebraska Medical Center · US

Funding

The Role of Excitatory Input into the PVN on Increased Sympathetic Drive in HeartP01HL062222 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SCHULTZ, HAROLD D · 1999 to 2019
$32.2M
Training Program in Hypertension, Kidney Disease & Cell BiologyT32DK007690 · NIDDK · UNIVERSITY OF IOWA · PI HUANG, CHOU-LONG, RAHMOUNI, KAMAL · 1992 to 2022
$2.8M
NHLBI NIH HHS P01 HL062222NHLBI NIH HHS P0-1 HL-62222NIDDK NIH HHS T32 DK007690
6 · The paper itself

Abstract

Excessive sympathetic drive is a hallmark of chronic heart failure (HF). Disease progression can be correlated with plasma norepinephrine concentration. Renal function is also correlated with disease progression and prognosis. Because both the renal nerves and renin-angiotensin II system are activated in chronic HF we hypothesized that excessive renal sympathetic nerve activity decreases renal blood flow in HF and is associated with changes in angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R) expression. The present study was carried out in conscious, chronically instrumented rabbits with pacing-induced HF. We found that rabbits with HF showed a decrease in mean renal blood flow (19.8±1.6 in HF vs. 32.0±2.5 ml/min from prepace levels; P<0.05) and an increase in renal vascular resistance (3.26±0.29 in HF vs. 2.21±0.13 mmHg·ml(-1)·min in prepace normal rabbits; P<0.05) while the blood flow and resistance was not changed in HF rabbits with the surgical renal denervation. Renal AT1R expression was increased by ∼67% and AT2R expression was decreased by ∼87% in rabbits with HF; however, kidneys from denervated rabbits with HF showed a near normalization in the expression of these receptors. These results suggest renal sympathetic nerve activity elicits a detrimental effect on renal blood flow and may be associated with alterations in the expression of angiotensin II receptors.

Indexed as

AnimalsDenervationHeart FailureKidneyKidney CortexMaleNorepinephrineRabbitsReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Receptors, AngiotensinRenal CirculationSmokeVascular ResistanceNorepinephrineReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Receptors, AngiotensinSmoke

Identifiers

PMID20962112
PMCPMC3023215
OpenAlexW2064800823

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.