Evidence map›Paper›PMID 21900645›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2011

Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus.

Marcia Venegas-Pont, Keisa W Mathis, Radu Iliescu, William H Ray, Porter H Glover, Michael J Ryan

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Exploration of ACE-Inhibiting Peptides Encrypted inBioMed research international · 2022
    Article
  3. Article
  4. Article
  5. Blood pressure and albuminuria in a female mouse model of systemic lupus erythematosus: impact of long-term high salt consumption.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Autoimmune Disease-Associated Hypertension.Current hypertension reports · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Understanding mechanisms of hypertension in systemic lupus erythematosus.Therapeutic advances in cardiovascular disease · 2016
    Review
  18. An impaired neuroimmune pathway promotes the development of hypertension in systemic lupus erythematosus.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
    Review
  19. Article
  20. Review
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

6 authors at 1 institution in 2 countries.

Marcia Venegas-PontDepartment of Physiology and Biophysics and Center for Excellence in Cardiovascular Renal Research, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA.
Keisa W Mathis
Radu Iliescu
William H Ray
Porter H Glover
Michael J Ryan
University of Mississippi Medical Center · US

Funding

Blood Pressure, Renal Hemodynamics, and InflammationR01HL085907 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI RYAN, MICHAEL · 2007 to 2011
$1.7M
Blood Pressure, Renal Hemodynamics, and InflammationK02HL092284 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI RYAN, MICHAEL · 2008 to 2011
$311k
IL-1RA INHIBITION OF IL-1 BETA&TNF - ALPHA PRODUCTIONF32HL008590 · NHLBI · OHIO STATE UNIVERSITY · PI MARSH, CLAY B · 1992 to 1993
–
NHLBI NIH HHS HL085907NHLBI NIH HHS HL085907S3NHLBI NIH HHS HL092284NHLBI NIH HHS P01HL5197
6 · The paper itself

Abstract

Inflammation and immune system dysfunction contributes to the development of cardiovascular and renal disease. Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that carries a high risk for both renal and cardiovascular disease. While hemodynamic changes that may contribute to increased cardiovascular risk have been reported in humans and animal models of SLE, renal hemodynamics have not been widely studied. The renin-angiotensin system (RAS) plays a central role in renal hemodynamic control, and although RAS blockade is a common therapeutic strategy, the role of RAS in hemodynamic function during SLE is not clear. This study tested whether mean arterial pressure (MAP) and renal hemodynamic responses to acute infusions of ANG II in anesthetized animals were enhanced in an established female mouse model of SLE (NZBWF1). Baseline MAP was not different between anesthetized SLE and control (NZWLacJ) mice, while renal blood flow (RBF) was significantly lower in mice with SLE. SLE mice exhibited an enhanced pressor response and greater reduction in RBF after ANG II infusion. An acute infusion of the ANG II receptor blocker losartan increased RBF in control mice but not in mice with SLE. Renin and ANG II type 1 receptor expression was significantly lower, and ANG II type 2 receptor expression was increased in the renal cortex from SLE mice compared with controls. These data suggest that there are fewer ANG II receptors in the kidneys from mice with SLE but that the existing receptors exhibit an enhanced sensitivity to ANG II.

Indexed as

Blood PressureRenal CirculationAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsAntihypertensive AgentsDisease Models, AnimalFemaleHypertensionInfusions, Intra-ArterialKidneyLosartanLupus Erythematosus, SystemicMiceMice, Inbred NZBReceptor, Angiotensin, Type 1Angiotensin IIAngiotensin II Type 1 Receptor BlockersAntihypertensive AgentsLosartanReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2RNA, Messenger

Identifiers

PMID21900645
PMCPMC3213953
OpenAlexW2092621548

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.