Evidence map›Paper›PMID 21345976›Full record

ReviewAmerican journal of physiology. Renal physiology2011

Luminal flow regulates NO and O2(-) along the nephron.

Pablo D Cabral, Jeffrey L Garvin

Open access · greenAbstract readReview
In one paragraph

Review 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. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
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  7. Article
  8. Review
  9. Tubule-vascular feedback in renal autoregulation.American journal of physiology. Renal physiology · 2019
    Review
  10. Article
  11. Sexual Dimorphic Pattern of Renal Transporters and Electrolyte Homeostasis.Journal of the American Society of Nephrology : JASN · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. An emerging role for gasotransmitters in the control of breathing and ionic regulation in fish.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2016
    Review
  17. Review
  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

2 authors at 1 institution in 1 country.

Pablo D CabralHypertension and Vascular Research Div., Dept. of Internal Medicine, Henry Ford Hospital, Detroit, MI 48202, USA.
Jeffrey L Garvin
Henry Ford Hospital · US

Funding

VASOACTIVE HORMONES IN THE REGULATION OF BLOOD PRESSUREP01HL028982 · NHLBI · HENRY FORD HOSPITAL · PI ORTIZ, PABLO A. · 1985 to 2017
$39.8M
Tubuloglomerular Feedback Regulation by Carbon MonoxideP01HL090550 · NHLBI · HENRY FORD HEALTH SYSTEM · PI ORTIZ, PABLO A. · 2009 to 2013
$10.2M
Salt-Sensitive Hypertension: Role of Renal SuperoxideR01HL070985 · NHLBI · HENRY FORD HEALTH SYSTEM · PI Jeffrey L. Garvin · 2002 to 2026
$6.3M
NHLBI NIH HHS HL 028982NHLBI NIH HHS HL 070985NHLBI NIH HHS HL 090550NHLBI NIH HHS P01 HL028982NHLBI NIH HHS R01 HL070985
6 · The paper itself

Abstract

Urinary flow is not constant but in fact highly variable, altering the mechanical forces (shear stress, stretch, and pressure) exerted on the epithelial cells of the nephron as well as solute delivery. Nitric oxide (NO) and superoxide (O(2)(-)) play important roles in various processes within the kidney. Reductions in NO and increases in O(2)(-) lead to abnormal NaCl and water absorption and hypertension. In the last few years, luminal flow has been shown to be a regulator of NO and O(2)(-) production along the nephron. Increases in luminal flow enhance fluid, Na, and bicarbonate transport in the proximal tubule. However, we know of no reports directly addressing flow regulation of NO and O(2)(-) in this segment. In the thick ascending limb, flow-stimulated NO and O(2)(-) formation has been extensively studied. Luminal flow stimulates NO production by nitric oxide synthase type 3 and its translocation to the apical membrane in medullary thick ascending limbs. These effects are mediated by flow-induced shear stress. In contrast, flow-induced stretch and NaCl delivery stimulate O(2)(-) production by NADPH oxidase in this segment. The interaction between flow-induced NO and O(2)(-) is complex and involves more than one simply scavenging the other. Flow-induced NO prevents flow from increasing O(2)(-) production via cGMP-dependent protein kinase in thick ascending limbs. In macula densa cells, shear stress increases NO production and this requires that the primary cilia be intact. The role of luminal flow in NO and O(2)(-) production in the distal tubule is not known. In cultured inner medullary collecting duct cells, shear stress enhances nitrite accumulation, a measure of NO production. Although much progress has been made on this subject in the last few years, there are still many unanswered questions.

Indexed as

Mechanotransduction, CellularUrodynamicsAnimalsHumansNADPH OxidasesNephronsNitric OxideNitric Oxide Synthase Type IIIPressureSodium Chloride, DietaryStress, MechanicalSuperoxidesNADPH OxidasesNitric OxideNitric Oxide Synthase Type IIISodium Chloride, DietarySuperoxides

Identifiers

PMID21345976
PMCPMC3094045
OpenAlexW1933660351

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.