Evidence map›Paper›PMID 20933519›Full record

ArticleJournal of molecular and cellular cardiology2011

Pravastatin normalises peripheral cardiac sympathetic hyperactivity in the spontaneously hypertensive rat.

Neil Herring, Chee Wan Lee, Nicholas Sunderland, Kathryn Wright, David J Paterson

Open access · hybridAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Statin therapy lowers muscle sympathetic nerve activity and oxidative stress in patients with heart failure.American journal of physiology. Heart and circulatory physiology · 2012
    Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Dysregulation of Neuronal Ca2+ Channel Linked to Heightened Sympathetic Phenotype in Prohypertensive States.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  12. Cardiac sympatho-vagal balance and ventricular arrhythmia.Autonomic neuroscience : basic & clinical · 2016
    Review
  13. Review
  14. Article
  15. Cardiac NO signalling in the metabolic syndrome.British journal of pharmacology · 2015
    Review
  16. Article
  17. Peripheral cardiac sympathetic hyperactivity in cardiovascular disease: role of neuropeptides.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Review
  18. Cardiac sympathetic dysfunction in the prehypertensive spontaneously hypertensive rat.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Neil HerringBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, OX1 3PT, UK. neilherring@doctors.org.uk
Chee Wan Lee
Nicholas Sunderland
Kathryn Wright
David J Paterson
University of Oxford · GB

Funding

British Heart Foundation
6 · The paper itself

Abstract

Hypertension is associated with heightened cardiac sympathetic drive whilst statins reduce angiotensin II (ATII) signalling, superoxide anion production and increase nitric oxide bioavailability, events that can potentially reduce peripheral cardiac sympathetic neurotransmission. We therefore investigated whether pravastatin alters peripheral cardiac sympathetic control in the spontaneously hypertensive rat (SHR). SHRs (16-18 weeks) had significantly (p<0.05) enhanced atrial (3)H-norepinephrine ((3)H-NE) release to field stimulation compared to normotensive WKYs. 2-week pravastatin supplementation significantly reduced (3)H-NE release to levels observed in the WKY. In-vivo, pravastatin lowered resting heart rate (HR) in the SHR despite not affecting arterial blood pressure or serum cholesterol. In SHR atria/right stellate ganglion preparations, the HR response to stellate stimulation (1, 3, and 5 Hz) was also significantly reduced by pravastatin whilst the HR response to exogenous NE (0.025-5 μmol) remained similar. The nitric oxide synthase (NOS) inhibitor l-NAME (1 mmol/l) increased (3)H-NE release by similar amounts in atria from supplemented and non-supplemented SHRs, whilst Western blotting showed no difference in protein levels of nNOS, eNOS, guanylyl cyclase, or the NADPH oxidase subunits Gp91 and P40 phox. Pravastatin significantly reduced cardiac ATII levels and angiotensin converting enzyme 1 and 2 expressions whilst protein levels of the ATII receptor (ATR(1)) remained unchanged in the SHR. Immunohistochemistry co-localised ATR(1) with tyrosine hydroxylase positive neurons in the stellate ganglion. The ATR(1) antagonist Losartan (5 μmol) equalised release of (3)H-NE to comparable levels in supplemented and non-supplemented SHRs. These results suggest 2-week pravastatin treatment reduces cardiac ATII, and prevents its facilitatory effect on NE release thus normalising cardiac sympathetic hyper-responsiveness in SHRs.

Indexed as

AnimalsBlotting, WesternCholesterolGuanylate CyclaseHeart RateImmunohistochemistryLosartanMaleNADPH OxidasesNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type INitric Oxide Synthase Type IIIPeptidyl-Dipeptidase APravastatinCholesterolGuanylate CyclaseLosartanNADPH OxidasesNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type INitric Oxide Synthase Type IIIPeptidyl-Dipeptidase APravastatinReceptors, AngiotensinTyrosine 3-Monooxygenase

Identifiers

PMID20933519
PMCPMC3020274
OpenAlexW1965559087

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.