Evidence map›Paper›PMID 22252398›Full record

ArticleHypertension (Dallas, Tex. : 1979)2012

Abnormal intracellular calcium homeostasis in sympathetic neurons from young prehypertensive rats.

Dan Li, Chee-wan Lee, Keith Buckler, Anant Parekh, Neil Herring, David J Paterson

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.2field-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

40 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023
    Review
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  19. Prevention of Injury-Induced Osteoarthritis in Rodent Temporomandibular Joint by Targeting Chondrocyte CaSR.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  20. Pre-emptive medicine for hypertension and its prospects.Hypertension research : official journal of the Japanese Society of Hypertension · 2019
    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

6 authors at 1 institution in 1 country.

Dan LiBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy, and Genetics, Oxford, UK. dan.li@dpag.ox.ac.uk
Chee-wan Lee
Keith Buckler
Anant Parekh
Neil Herring
David J Paterson
British Heart Foundation · GB

Funding

British Heart Foundation PG/08/061British Heart Foundation PG/08/061/25380British Heart Foundation PG/11/5/28643Wellcome Trust 084655
6 · The paper itself

Abstract

Hypertension is associated with cardiac noradrenergic hyperactivity, although it is not clear whether this precedes or follows the development of hypertension itself. We hypothesized that Ca(2+) homeostasis in postganglionic sympathetic neurons is impaired in spontaneously hypertensive rats (SHRs) and may occur before the development of hypertension. The depolarization-induced rise in intracellular free calcium concentration ([Ca(2+)](i); measured using fura-2-acetoxymethyl ester) was significantly larger in cultured sympathetic neurons from prehypertensive SHRs than in age matched normotensive Wistar-Kyoto rats. The decay of the [Ca(2+)](i) transient was also faster in SHRs. The endoplasmic reticulum Ca(2+) content and caffeine-induced [Ca(2+)](i) amplitude were significantly greater in the young SHRs. Lower protein levels of phospholamban and more copies of ryanodine receptor mRNA were also observed in the young SHRs. Depleting the endoplasmic reticulum Ca(2+) store did not alter the difference of the evoked [Ca(2+)](i) transient and decay time between young SHRs and Wistar-Kyoto rats. However, removing mitochondrial Ca(2+) buffering abolished these differences. A lower mitochondrial membrane potential was also observed in young SHR sympathetic neurons. This resulted in impaired mitochondrial Ca(2+) uptake and release, which might partly be responsible for the increased [Ca(2+)](i) transient and faster decay in SHR sympathetic neurons. This Ca(2+) phenotype seen in early development in cardiac stellate and superior cervical ganglion neurons may contribute to the sympathetic hyperresponsiveness that precedes the onset of hypertension.

Indexed as

AnimalsCalciumCells, CulturedDisease Models, AnimalEndoplasmic ReticulumIntracellular FluidMaleMitochondriaNeuronsPrehypertensionRatsRats, Inbred SHRRats, Inbred WKYSympathetic Nervous SystemCalcium

Identifiers

PMID22252398
PMCPMC3299568
OpenAlexW2165424279

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.