Evidence map›Paper›PMID 19001187›Full record

ArticleHypertension (Dallas, Tex. : 1979)2008

Angiotensin II-dependent hypertension increases Na transport-related oxygen consumption by the thick ascending limb.

Guillermo B Silva, Jeffrey L Garvin

Open access · greenAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Oxidative Stress and Hypertensive Diseases.The Medical clinics of North America · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Thick ascending limb of the loop of Henle.Clinical journal of the American Society of Nephrology : CJASN · 2014
    Review
  17. A radical approach to balancing the tides of tubular flow.American journal of physiology. Renal physiology · 2014
    Article
  18. Angiotensin II stimulates basolateral 50-pS K channels in the thick ascending limb.American journal of physiology. Renal physiology · 2014
    Article
  19. Article
  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.

Guillermo B SilvaDivision of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan 48202, USA.
Jeffrey L Garvin
Wayne State University · US

Funding

VASOACTIVE HORMONES IN THE REGULATION OF BLOOD PRESSUREP01HL028982 · NHLBI · HENRY FORD HOSPITAL · PI ORTIZ, PABLO A. · 1985 to 2017
$39.8M
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 28982NHLBI NIH HHS HL 70985NHLBI NIH HHS P01 HL028982NHLBI NIH HHS R01 HL070985
6 · The paper itself

Abstract

Renal medullary superoxide (O(2)(-)) increases in angiotensin (Ang) II-dependent hypertension. O(2)(-) increases thick ascending limb Na transport, but the effect of Ang II-dependent hypertension on the thick ascending limb is unknown. We hypothesized that Ang II-dependent hypertension increases thick ascending limb NaCl transport because of enhanced O(2)(-) production and increased protein kinase C (PKC) alpha activity. We measured the effect of Ang II-dependent hypertension on furosemide-sensitive oxygen consumption (a measure of Na transport), O(2)(-) production, and PKCalpha translocation (a measure of PKCalpha activity) in thick ascending limb suspensions. Ang II-dependent hypertension increased furosemide-sensitive oxygen consumption (26.2+/-1.0% versus 36.6+/-1.2% of total oxygen consumption; P<0.01). O(2)(-) was also increased (1.1+/-0.2 versus 3.2+/-0.5 nmol of O(2)(-)/min per milligram of protein; P<0.03) in thick ascending limbs. Unilateral renal infusion of Tempol decreased O(2)(-) (2.4+/-0.4 versus 1.2+/-0.2 nmol of O(2)(-)/min per milligram of protein; P<0.04) and furosemide-sensitive oxygen consumption (32.8+/-1.3% versus 24.0+/-2.1% of total oxygen consumption; P<0.01) in hypertensive rats. Tempol did not affect O(2)(-) or furosemide-sensitive oxygen consumption in normotensive controls and did not alter systolic blood pressure. Ang II-dependent hypertension increased PKCalpha translocation (5.7+/-0.3 versus 13.8+/-1.4 AU per milligram of protein; P<0.01). Unilateral renal infusion of Tempol reduced PKCalpha translocation (5.0+/-0.9 versus 10.4+/-2.6 AU per milligram of protein; P<0.04) in hypertensive rats. Unilateral renal infusion of the PKCalpha inhibitor Gö6976 reduced furosemide-sensitive oxygen consumption (37.4+/-1.5% versus 25.1+/-1.0% of total oxygen consumption; P<0.01) in hypertensive rats. We conclude that Ang II-dependent hypertension enhances thick ascending limb Na transport-related oxygen consumption by increasing O(2)(-) and PKCalpha activity.

Indexed as

Angiotensin IIAnimalsAntioxidantsCyclic N-OxidesFurosemideHypertension, RenalLoop of HenleMaleOxygen ConsumptionProtein Kinase C-alphaRatsRats, Sprague-DawleyReactive Oxygen SpeciesSodiumSodium Potassium Chloride Symporter InhibitorsSodium-Potassium-Chloride SymportersAngiotensin IIAntioxidantsCyclic N-OxidesFurosemideProtein Kinase C-alphaReactive Oxygen SpeciesSodiumSodium Potassium Chloride Symporter InhibitorsSodium-Potassium-Chloride SymportersSpin LabelstempolVasoconstrictor Agents

Identifiers

PMID19001187
PMCPMC2766242
OpenAlexW2164757969

What OpenQuestion holds

Textmetadata
LicenceTDM
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.