Evidence map›Paper›PMID 10903974›Full record

ArticleBritish journal of pharmacology2000

Comparison of enalapril and valsartan in cyclosporine A-induced hypertension and nephrotoxicity in spontaneously hypertensive rats on high-sodium diet.

M Lassila, P Finckenberg, A K Pere, L Krogerus, J Ahonen, H Vapaatalo, M L Nurminen

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
7.8field-weighted citation impact, top 3% 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

13 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  4. Article
  5. Cardiovascular effects of immunosuppression agents.Frontiers in cardiovascular medicine · 2022
    Review
  6. Article
  7. Angiotensin II blockade upregulates the expression of Klotho, the anti-ageing gene, in an experimental model of chronic cyclosporine nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2011
    Article
  8. Article
  9. Article
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  11. 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

7 authors at 4 institutions in 2 countries.

M LassilaInstitute of Biomedicine, Department of Pharmacology and Toxicology, University of Helsinki, Finland. Research Laboratory, Fourth Department of Surgery, Helsinki University Central Hospital, Helsinki, Finland. Department of Pathology, He.
P Finckenberg
A K Pere
L Krogerus
J Ahonen
H Vapaatalo
M L Nurminen
Helsinki University Hospital · FIInstitute for Biomedicine · ITUniversity of Helsinki · FIHerttoniemi Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. We compared the effects of the angiotensin converting enzyme (ACE) inhibitor enalapril and the angiotensin AT(1) receptor antagonist valsartan in cyclosporine A (CsA)-induced hypertension and nephrotoxicity in spontaneously hypertensive rats (SHR). 2. SHR (8 - 9 weeks old) on high-sodium diet were given CsA (5 mg kg(-1)d (-1) s.c. ) for 6 weeks. The rats were treated concomitantly either with enalapril (30 mg kg(-1)d (-1) p.o.) or valsartan (3 or 30 mg kg(-1) d (-1) p.o.). To evaluate the role of bradykinin in the action of enalapril, some rats received a bradykinin B(2) receptor antagonist icatibant (HOE 140, 500 microg kg(-1) d (-1) s.c.) during the last 2 weeks of enalapril treatment. 3. Blood pressure was recorded every second week by tail cuff method. Renal function was measured by serum creatinine, creatinine clearance and urinary excretion of proteins at the end of the experiment. The activity of the renal kallikrein-kinin system was estimated by urinary kallikrein excretion. 4. CsA caused hypertension, impaired renal function and induced morphological nephrotoxicity with glomerular damage and interstitial fibrosis. Enalapril and the lower dose of valsartan attenuated the CsA-induced hypertension to the same extent, while the higher dose of valsartan totally abolished it. Icatibant did not reduce the antihypertensive effect of enalapril. Urinary kallikrein excretion was similar in all groups. 5. Enalapril and valsartan equally prevented the CsA-induced deterioration of kidney function and morphology. 6. The renin-angiotensin but not the kallikrein-kinin system plays a crucial role in CsA-toxicity during high intake of sodium in SHR.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsAnimalsAntihypertensive AgentsBlood PressureBody WeightBradykininBradykinin Receptor AntagonistsCyclosporineDose-Response Relationship, DrugDrinkingEatingElectrolytesEnalaprilHeart RateHypertensionAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsAntihypertensive AgentsBradykininBradykinin Receptor AntagonistsCyclosporineElectrolytesEnalaprilicatibantKallikreinsReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Receptor, Bradykinin B2ReninSodium, DietaryTetrazolesValineValsartan

Identifiers

PMID10903974
PMCPMC1572182
OpenAlexW2085244419

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.