Evidence map›Paper›PMID 16223765›Full record

ArticleThe Journal of physiology2005

Nitric oxide blunts myogenic autoregulation in rat renal but not skeletal muscle circulation via tubuloglomerular feedback.

Armin Just, William J Arendshorst

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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.

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

21 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  11. Article
  12. Article
  13. Article
  14. Connecting tubule glomerular feedback antagonizes tubuloglomerular feedback in vivo.American journal of physiology. Renal physiology · 2010
    Article
  15. Glomerular hyperfiltration in adult sickle cell anemia: a frequent hemolysis associated feature.Clinical journal of the American Society of Nephrology : CJASN · 2010
    Article
  16. Review
  17. Article
  18. Possible mediators of connecting tubule glomerular feedback.Hypertension (Dallas, Tex. : 1979) · 2009
    Article
  19. Article
  20. Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms.American journal of physiology. Regulatory, integrative and comparative physiology · 2006
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Armin JustDepartment of Cell and Molecular Physiology, 6341 Medical Biomolecular Research Bldg, CB 7545, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7545, USA. just@med.unc.edu
William J Arendshorst
University of North Carolina at Chapel Hill · US

Funding

Renal Vascular Reactivity in HypertensionR01HL002334 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ARENDSHORST, WILLIAM J · 1985 to 2014
$6.8M
NHLBI NIH HHS HL-02334NHLBI NIH HHS R01 HL002334
6 · The paper itself

Abstract

This rat renal blood flow (RBF) study quantified the impact of nitric oxide synthase (NOS) inhibition on the myogenic response and the balance of autoregulatory mechanisms in the time domain following a 20 mmHg-step increase or decrease in renal arterial pressure (RAP). When RAP was increased, the myogenic component of renal vascular resistance (RVR) rapidly rose within the initial 7-10 s, exhibiting an approximately 5 s time constant and providing approximately 36% of perfect autoregulation. A secondary rise between 10 and 40 s brought RVR to 95% total autoregulatory efficiency, reflecting tubuloglomerular feedback (TGF) and possibly one or two additional mechanisms. The kinetics were similar after the RAP decrease. Inhibition of NOS (by l-NAME) increased RAP, enhanced the strength (79% autoregulation) and doubled the speed of the myogenic response, and promoted the emergence of RVR oscillations ( approximately 0.2 Hz); the strength (52%) was lower at control RAP. An equi-pressor dose of angiotensin II had no effect on myogenic or total autoregulation. Inhibition of TGF (by furosemide) abolished the l-NAME effect on the myogenic response. RVR responses during furosemide treatment, assuming complete inhibition of TGF, suggest a third mechanism that contributes 10-20% and is independent of TGF, slower than the myogenic response, and abolished by NOS inhibition. The hindlimb circulation displayed a solitary myogenic response similar to the kidney (35% autoregulation) that was not enhanced by l-NAME. We conclude that NO normally restrains the strength and speed of the myogenic response in RBF but not hindlimb autoregulation, an action dependent on TGF, thereby allowing more and slow RAP fluctuations to reach glomerular capillaries.

Indexed as

AnimalsDiureticsFurosemideHindlimbKidney GlomerulusMaleMuscle, SkeletalNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseRatsRats, Sprague-DawleyRegional Blood FlowRenal CirculationVasoconstrictionDiureticsFurosemideNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase

Identifiers

PMID16223765
PMCPMC1464274
OpenAlexW1525465974

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.