Evidence map›Paper›PMID 23160444›Full record

ReviewCurrent opinion in nephrology and hypertension2013

Nitric oxide and the A and B of endothelin of sodium homeostasis.

Kelly A Hyndman, Jennifer S Pollock

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021
    Article
  5. Article
  6. Oxidative stress induces BHBioscience reports · 2018
    Article
  7. Article
  8. Article
  9. 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
  10. Endothelin.Pharmacological reviews · 2016
    Review
  11. Article
  12. Collecting duct principal cell transport processes and their regulation.Clinical journal of the American Society of Nephrology : CJASN · 2015
    Review
  13. Inhibition of ENaC by endothelin-1.Vitamins and hormones · 2015
    Review
  14. Review
  15. Sex differences in ET-1 receptor expression and Ca2+ signaling in the IMCD.American journal of physiology. Renal physiology · 2013
    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.

Kelly A HyndmanDepartment of Medicine, Section of Experimental Medicine, Georgia Health Sciences University, Augusta, Georgia 30912, USA.
Jennifer S Pollock
Augusta University Health · US

Funding

Renal endothelin receptor-specific function in angiotensin ll-dependent hypertensP01HL095499 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POLLOCK, DAVID M · 2010 to 2014
$11.1M
Nitric Oxide Synthase Isoforms in the KidneyR01HL060653 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI POLLOCK, JENNIFER S · 1999 to 2010
$2.5M
NHLBI NIH HHS HL60653NHLBI NIH HHS HL95499NHLBI NIH HHS P01 HL095499NHLBI NIH HHS R01 HL060653
6 · The paper itself

Abstract

purpose of reviewIn recent years, renal collecting duct-specific endothelin-1 (ET1), endothelin A (ETA) and endothelin B (ETB) receptors as well as nitric oxide synthase 1 (NOS1) knockout mice have been developed with subsequent identification for an integral role in regulation of sodium water homeostasis and ultimately blood pressure. The focus of this review is to integrate these models and to propose a scheme for the control of sodium excretion by the collecting duct and the endothelin/ETB/NOS system. RECENT

findingsNOS1 splice variants are expressed in the kidney, especially in the collecting duct. Mice express predominantly NOS1β in the medulla, with NOS1α and NOS1β in the cortex, whereas rats express NOS1α and NOS1β in both the cortex and medulla. Novel transcription of collecting duct ET1 mediated by epithelial sodium channels, mitochondrial Na/Ca exchangers and glucocorticoids has been determined. ET1 via the ETB receptor increases nitric oxide production in both rat and mouse collecting ducts, suggesting that NOS1β is linked to ET1-dependent NOS activation in the kidney. As well, genetic deletion of NOS1 splice variants in the collecting duct results in a salt-sensitive hypertensive phenotype in mice, much like the collecting duct ET1 and collecting duct ETB knockout mice. SUMMARY: In the collecting duct, the ET1/nitric oxide pathways are intimately linked, and deletion of collecting duct ET1, ETB receptor or NOS1β results in a salt-sensitive phenotype, which is at least partially dependent on dysregulation of sodium and water reabsorption.

Indexed as

AnimalsEndothelin-1HomeostasisHumansKidney Tubules, CollectingModels, AnimalNitric Oxide Synthase Type ISignal TransductionSodiumWaterEndothelin-1Nitric Oxide Synthase Type INos1 protein, mouseSodiumWater

Identifiers

PMID23160444
PMCPMC3897245
OpenAlexW2071499394

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.