Evidence map›Paper›PMID 35722114›Full record

ArticleFrontiers in cardiovascular medicine2022

Evidence for a Prehypertensive Water Dysregulation Affecting the Development of Hypertension: Results of Very Early Treatment of Vasopressin V1 and V2 Antagonism in Spontaneously Hypertensive Rats.

Ignazio Verzicco, Stefano Tedeschi, Gallia Graiani, Alice Bongrani, Maria Luisa Carnevali, Simona Dancelli, Jessica Zappa, Silvia Mattei, Achiropita Bovino, Stefania Cavazzini and 8 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

18 authors at 3 institutions in 1 country.

Ignazio VerziccoCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Stefano TedeschiCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Gallia GraianiHistology and Histopathology Unit and Molecular Biology Laboratory, Dental School Parma, University of Parma, Parma, Italy.
Alice BongraniCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Maria Luisa CarnevaliCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Simona DancelliCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Jessica ZappaCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Silvia MatteiNefrologia e Dialisi, Azienda USL - Istituto di Ricerca a Carattere Scientifico IRCCS Reggio Emilia, Reggio Emilia, Italy.
Achiropita BovinoInternal Medicine Unit, Ospedale Fidenza, Azienda USL Parma, Parma, Italy.
Stefania CavazziniLaboratory of Industrial Toxicology, DIMEC, University of Parma, Parma, Italy.
Rossana RoccoCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Anna CalviCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Barbara PalladiniCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Riccardo VolpiCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Valentina CannoneCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Pietro CoghiCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Alberico BorghettiCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
Aderville CabassiCardiorenal and Hypertension Research Unit, Physiopathology Unit, Clinica Medica Generale e Terapia Medica, Department of Medicine and Surgery (DIMEC), University of Parma, Parma, Italy.
University of Parma · ITAzienda Sanitaria Unità Locale di Reggio Emilia · ITOspedale di Parma · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to long-term regulation of blood pressure (BP), in the kidney resides the initial trigger for hypertension development due to an altered capacity to excrete sodium and water. Betaine is one of the major organic osmolytes, and its betaine/gamma-aminobutyric acid transporter (BGT-1) expression in the renal medulla relates to interstitial tonicity and urinary osmolality and volume. This study investigated altered water and sodium balance as well as changes in antidiuretic hormone (ADH) activity in female spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats from their 3-5 weeks of age (prehypertensive phase) to SHR's 28-30 weeks of age (established hypertension-organ damage). Young prehypertensive SHRs showed a reduced daily urine output, an elevated urine osmolarity, and higher immunostaining of tubule BGT-1, alpha-1-Na-K ATPase in the outer medulla vs. age-matched WKY. ADH circulating levels were not different between young prehypertensive SHR and WKY, but the urine aquaporin2 (AQP2)/creatinine ratio and labeling of AQP2 in the collecting duct were increased. At 28-30 weeks, hypertensive SHR with moderate renal failure did not show any difference in urinary osmolarity, urine AQP2/creatinine ratio, tubule BGT-1, and alpha-1-Na-K ATPase as compared with WKY. These results suggest an increased sensitivity to ADH in prehypertensive female SHR. On this basis, a second series of experiments were set to study the role of ADH V1 and V2 receptors in the development of hypertension, and a group of female prehypertensive SHRs were treated from the 25th to 49th day of age with either V1 (OPC21268) or V2 (OPC 41061) receptor antagonists to evaluate the BP time course. OPC 41061-treated SHRs had a delayed development of hypertension for 5 weeks without effect in OPC 21268-treated SHRs. In prehypertensive female SHR, an increased renal ADH sensitivity is crucial for the development of hypertension by favoring a positive water balance. Early treatment with selective V2 antagonism delays future hypertension development in young SHRs.

Indexed as

aquaporin 2experimental hypertensionpre-hypertensive phasespontaneously hypertensive ratvasopressinvasopressin receptor 1 and 2 antagonism

Identifiers

PMID35722114
PMCPMC9198251
OpenAlexW4281907559

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.