Evidence map›Paper›PMID 18391099›Full record

ArticleHypertension (Dallas, Tex. : 1979)2008

Collecting duct-derived endothelin regulates arterial pressure and Na excretion via nitric oxide.

Markus P Schneider, Yuqiang Ge, David M Pollock, Jennifer S Pollock, Donald E Kohan

Open access · bronzeAbstract 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 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 87 citations in OpenAlex.

  1. Trial
  2. Article
  3. Sex-Specific Differences in Kidney Function and Blood Pressure Regulation.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Current perspective on circadian function of the kidney.American journal of physiology. Renal physiology · 2024
    Review
  6. Article
  7. Article
  8. Circadian Control of Sodium and Blood Pressure Regulation.American journal of hypertension · 2021
    Review
  9. High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021
    Article
  10. Review
  11. Article
  12. Nitric oxide production by glomerular podocytes.Nitric oxide : biology and chemistry · 2018
    Article
  13. Renal denervation attenuates hypertension but not salt sensitivity in ETAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Role of endothelin-1 for the regulation of renal pelvic function.Pflugers Archiv : European journal of physiology · 2016
    Article
  18. High salt induces autocrine actions of ET-1 on inner medullary collecting duct NO production via upregulated ETB receptor expression.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  19. Dual inhibition of renin-angiotensin-aldosterone system and endothelin-1 in treatment of chronic kidney disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Review
  20. Endothelin.Pharmacological reviews · 2016
    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

5 authors at 1 institution in 1 country.

Markus P SchneiderVascular Biology Center, Medical College of Georgia, Augusta, USA.
Yuqiang Ge
David M Pollock
Jennifer S Pollock
Donald E Kohan
Augusta University · US

Funding

Vascular Rho-kinase Signaling in Angiotensin II hypertenP01HL074167 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI BRANDS, MICHAEL W. · 2004 to 2008
$10.5M
Nitric Oxide Synthase Isoforms in the KidneyR01HL060653 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI POLLOCK, JENNIFER S · 1999 to 2010
$2.5M
ENDOTHELIN REGULATION OF KIDNEY FUNCTIONR01HL064776 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI POLLOCK, DAVID M · 2000 to 2007
$1.6M
Physiologic role of collecting duct ciiliary proteinsR21DK075362 · NIDDK · UNIVERSITY OF UTAH · PI KOHAN, DONALD E · 2006 to 2007
$405k
NHLBI NIH HHS HL 60653NHLBI NIH HHS HL 64776NHLBI NIH HHS HL 74167NHLBI NIH HHS P01 HL074167NHLBI NIH HHS R01 HL060653NHLBI NIH HHS R01 HL064776NIDDK NIH HHS DK075362NIDDK NIH HHS DK96392NIDDK NIH HHS R21 DK075362
6 · The paper itself

Abstract

Mice with a collecting duct-specific deletion of endothelin-1 are hypertensive and have impaired Na excretion. Because endothelin-1 activates NO synthase (NOS) in the collecting duct, we hypothesized that impaired renal NO production in knockout mice exacerbates the hypertensive state. Control and knockout mice were treated chronically with N(G)-nitro-l-arginine methyl ester, and blood pressure (BP) and urinary nitrate/nitrite excretion were assessed. On a normal Na diet, knockout systolic BP was 18 mm Hg greater than in controls. N(G)-nitro-l-arginine methyl ester increased BP in control mice by 30 mm Hg and 10 mm Hg in collecting duct-specific deletion of endothelin-1 knockout mice, thereby abolishing the difference in systolic BP between the groups. A high-Na diet increased BP similarly in both groups. Urinary nitrate/nitrite excretion was lower in knockout mice than in controls on normal or high Na intake. In separate experiments, renal perfusion pressure was adjusted in anesthetized mice, and urinary nitrate/nitrite and Na excretion were determined. Similar elevations of BP increased urinary Na and nitrate/nitrite excretion in control mice but to a significantly lesser extent in knockout mice. Isoform-specific NOS activity and expression were determined in renal inner medulla homogenates from control and knockout mice. NOS1 and NOS3 activities were lower in knockout than in control mice given normal or high-Na diets. However, NOS1 or NOS3 protein expressions were similar in both groups on normal or high-Na intake. These data demonstrate that collecting duct-derived endothelin-1 is important in the following: (1) chronic N(G)-nitro-l-arginine methyl ester-induced hypertension; (2) full expression of pressure-dependent changes in sodium excretion; and (3) control of inner medullary NOS1 and NOS3 activity.

Indexed as

AnimalsBlood PressureDiuresisEndothelin-1Enzyme InhibitorsHeart RateHypertension, RenalKidney MedullaKidney Tubules, CollectingMiceMice, KnockoutNatriuresisNG-Nitroarginine Methyl EsterNitratesNitric OxideNitric Oxide Synthase Type IEndothelin-1Enzyme InhibitorsNG-Nitroarginine Methyl EsterNitratesNitric OxideNitric Oxide Synthase Type INitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitritesNos1 protein, mouseNos3 protein, mouseSodium

Identifiers

PMID18391099
PMCPMC3799791
OpenAlexW2137458614

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.