Evidence map›Paper›PMID 31430751›Full record

ArticleKidney & blood pressure research2019

Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure.

Šárka Vacková, Soňa Kikerlová, Vojtěch Melenovsky, František Kolář, John D Imig, Elzbieta Kompanowska-Jezierska, Janusz Sadowski, Luděk Červenka

Open access · goldAbstract read
In one paragraph

Article in Kidney & blood pressure research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

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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

8 authors at 4 institutions in 3 countries.

Šárka VackováCenter for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czechia.
Soňa KikerlováCenter for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czechia.
Vojtěch MelenovskyDepartment of Cardiology, Institute for Clinical and Experimental Medicine, Prague, Czechia.
František KolářDepartment of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czechia.
John D ImigDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Elzbieta Kompanowska-JezierskaDepartment of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Science, Warsaw, Poland.
Janusz SadowskiDepartment of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Science, Warsaw, Poland.
Luděk ČervenkaCenter for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czechia, luce@medicon.cz.
Institute of Clinical and Experimental Medicine · CZMossakowski Medical Research Institute, Polish Academy of Sciences · PLCzech Academy of Sciences, Institute of Physiology · CZMedical College of Wisconsin · US

Funding

Eicosanoid-based Therapy for DiabetesR01DK103616 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI IMIG, JOHN D · 2015 to 2019
$2.4M
NIDDK NIH HHS R01 DK103616
6 · The paper itself

Abstract

objectiveWe evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acids (EETs).

methodsRen-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation).

resultsSelective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR.

conclusionThe findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF.

Indexed as

Angiotensin IIAnimalsArterio-Arterial FistulaHeart FailureHypertensionPulmonary ArteryRatsRats, TransgenicRenal CirculationVasoconstrictionVasoconstrictor AgentsVasodilationAngiotensin IIVasoconstrictor AgentsAcetylcholineAngiotensin IIAorto-caval fistulaBradykininCongestive heart failureEpoxyeicosatrienoic acidHypertensionNorepinephrineRenal blood flowRenal dysfunctionRenal vascular reactivity

Identifiers

PMID31430751
PMCPMC10107072
OpenAlexW2970685566

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.