Evidence map›Paper›PMID 19617413›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

Low-dose ouabain constricts small arteries from ouabain-hypertensive rats: implications for sustained elevation of vascular resistance.

Jin Zhang, John M Hamlyn, Eiji Karashima, Hema Raina, Joseph R H Mauban, Michelle Izuka, Roberto Berra-Romani, Alessandra Zulian, W Gil Wier, Mordecai P Blaustein

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  8. Pivotal role of α2 NaThe Journal of physiology · 2016
    Review
  9. Review
  10. Article
  11. Salt sensitivity, endogenous ouabain and hypertension.Current opinion in nephrology and hypertension · 2013
    Review
  12. Article
  13. Article
  14. How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension.American journal of physiology. Heart and circulatory physiology · 2012
    Review
  15. Article
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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

10 authors at 1 institution in 1 country.

Jin ZhangDepartment of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA. jzhan002@umaryland.edu
John M Hamlyn
Eiji Karashima
Hema Raina
Joseph R H Mauban
Michelle Izuka
Roberto Berra-Romani
Alessandra Zulian
W Gil Wier
Mordecai P Blaustein
University of Maryland, Baltimore · US

Funding

Sympathetic Neurotransmitters and Ouabain HypertensionP01HL078870 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BLAUSTEIN, MORDECAI P · 2005 to 2009
$9.9M
NHLBI NIH HHS P01-HL-78870
6 · The paper itself

Abstract

Prolonged ouabain administration to normal rats causes sustained blood pressure (BP) elevation. This ouabain-induced hypertension (OH) has been attributed, in part, to the narrowing of third-order resistance arteries (approximately 320 microm internal diameter) as a result of collagen deposition in the artery media. Here we describe the structural and functional properties of fourth-order mesenteric small arteries from control and OH rats, including the effect of low-dose ouabain on myogenic tone in these arteries. Systolic BP in OH rats was 138 +/- 3 versus 124 +/- 4 mmHg in controls (P < 0.01). Pressurized (70 mmHg) control and OH arteries, with only a single layer of myocytes, both had approximately 165-microm internal diameters and approximately 20-microm wall thicknesses. Even after fixation, despite vasoconstriction, the diameters and wall thicknesses did not differ between control and OH fourth-order arteries, whereas in third-order arteries, both parameters were significantly smaller in OH than in controls. Myogenic reactivity was significantly augmented in OH fourth-order arteries. Nevertheless, phenylephrine- (1 microM) and high K(+)-induced vasoconstrictions and acetylcholine-induced vasodilation were comparable in control and OH arteries. Vasoconstrictions induced by 5 microM phenylephrine and by 10 mM caffeine in Ca(2+)-free media indicated that releasable sarcoplasmic reticulum Ca(2+) stores were normal in OH arteries. Importantly, 100 nM ouabain constricted both control and OH arteries by approximately 26 microm, indicating that this response was not downregulated in OH rats. This maximal ouabain-induced constriction corresponds to a approximately 90% increase in resistance to flow in these small arteries; thus ouabain at EC(50) of approximately 0.66 nM should raise resistance by approximately 35%. We conclude that dynamic constriction in response to circulating nanomolar ouabain in small arteries likely makes a major contribution to the increased vascular tone and BP in OH rats.

Indexed as

AcetylcholineAnimalsBlood PressureCaffeineCalciumDose-Response Relationship, DrugEnzyme InhibitorsHypertensionMaleMesenteric ArteriesOuabainPhenylephrinePhosphodiesterase InhibitorsPotassiumRatsRats, Sprague-DawleyAcetylcholineCaffeineCalciumEnzyme InhibitorsOuabainPhenylephrinePhosphodiesterase InhibitorsPotassiumVasoconstrictor AgentsVasodilator Agents

Identifiers

PMID19617413
PMCPMC2755988
OpenAlexW2112534969

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.