Evidence map›Paper›PMID 23011292›Full record

ArticleClinical and experimental nephrology2013

Additive effects of cilnidipine and angiotensin II receptor blocker in preventing the progression of diabetic nephropathy in diabetic spontaneously hypertensive rats.

Shizuka Aritomi, Kazumi Niinuma, Tetsuya Ogawa, Tomoyuki Konda, Kosaku Nitta

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Clinical and experimental nephrology, 2013. 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
0.6field-weighted citation impact, top 28% 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, 8 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

5 authors at 3 institutions in 1 country.

Shizuka AritomiResearch Center, Ajinomoto Pharmaceuticals Co., Ltd., Kanagawa, Japan.
Kazumi Niinuma
Tetsuya Ogawa
Tomoyuki Konda
Kosaku Nitta
Ajinomoto (Japan) · JPTokyo Women's Medical University · JPTokyo Women's Medical University Adachi Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCilnidipine (Cil) is an L/N-type calcium channel blocker (CCB) that is known to provide renal protection by decreasing the activity of the sympathetic nervous system and the renin-angiotensin system (RAS). However, very few studies have evaluated the renoprotective effects of Cil in hypertension complicated by diabetes mellitus. In this study, we compared the effects of cilnidipine and the L-type CCB, amlodipine (Aml), in combination with an angiotensin II receptor blocker (ARB) on diabetic nephropathy that developed as a result of inducing diabetes in hypertensive rats.

methodsDiabetes was induced in 9-week-old male spontaneously hypertensive rats by intraperitoneally injecting them with streptozotocin (40 mg/kg twice) and the rats (8 per group) were randomly assigned to receive valsartan (Val), Cil + Val, Aml + Val, or vehicle for 8 weeks through a gastric tube.

resultsThere were no significant differences in systolic blood pressure or plasma parameters between the two combination therapy groups. Blood pressure lowering by neither combination therapy significantly affected the glycemic variables. However, the increased glycogen levels in the kidney as a result of hyperglycemia were significantly suppressed in the groups that received combination therapy, and the increased proteinurea and glomerulosclerosis due to progression of the diabetic nephropathy were significantly suppressed in the Cil + Val group. In addition, a significant decrease in ED-1-positive cells was observed in the Cil + Val group alone.

conclusionThe results of this study suggested that the L/N-type CCB, cilnidipine, had additive antihypertensive and proteinuria-lowering effects when administered in combination with an ARB, even in type-1 diabetic rats, and that the L-type CCB, amlodipine, did not. Furthermore, combination therapy with cilnidipine and valsartan significantly reduced glycogen accumulation and ED-1-positive cell infiltration, suggesting that cilnidipine suppressed the excessive increase in the activity of the sympathetic nervous system and RAS through N-type calcium channel blockade.

Indexed as

AmlodipineAngiotensin II Type 1 Receptor BlockersAnimalsAntihypertensive AgentsBiomarkersBlood GlucoseBlood PressureCalcium Channel BlockersDiabetes Mellitus, ExperimentalDiabetic NephropathiesDihydropyridinesDisease ProgressionDrug Therapy, CombinationGlomerulonephritisGlucagonGlucose Transporter Type 1AmlodipineAngiotensin II Type 1 Receptor BlockersAntihypertensive AgentsBiomarkersBlood GlucoseCalcium Channel BlockerscilnidipineDihydropyridinesGlucagonGlucose Transporter Type 1Glycated HemoglobinGlycogenhemoglobin A1c protein, humanNorepinephrineSlc2a1 protein, ratTetrazolesTgfb1 protein, ratTransforming Growth Factor beta1ValineValsartan

Identifiers

PMID23011292
OpenAlexW2031753103

What OpenQuestion holds

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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.