Evidence map›Paper›PMID 24970998›Full record

ArticleDrug design, development and therapy2014

Additive effects of cilnidipine, an L-/N-type calcium channel blocker, and an angiotensin II receptor blocker on reducing cardiorenal damage in Otsuka Long-Evans Tokushima Fatty rats with type 2 diabetes mellitus.

Yutaka Mori, Shizuka Aritomi, Kazumi Niinuma, Tarou Nakamura, Kenichi Matsuura, Junichi Yokoyama, Kazunori Utsunomiya

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2014. 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 33% 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.

  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

7 authors at 3 institutions in 1 country.

Yutaka MoriDivision of Diabetes and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Minato-ku, Japan ; Department of Clinical Research, National Hospital Organization, Utsunomiya National Hospital, Utsunomiya, Japan.
Shizuka AritomiResearch Center, Ajinomoto Pharmaceuticals Co, Ltd, Kanagawa, Japan.
Kazumi NiinumaResearch Center, Ajinomoto Pharmaceuticals Co, Ltd, Kanagawa, Japan.
Tarou NakamuraResearch Center, Ajinomoto Pharmaceuticals Co, Ltd, Kanagawa, Japan.
Kenichi MatsuuraDivision of Diabetes and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Minato-ku, Japan.
Junichi YokoyamaDivision of Diabetes and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Minato-ku, Japan.
Kazunori UtsunomiyaDivision of Diabetes and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Minato-ku, Japan.
Ajinomoto (Japan) · JPJikei University School of Medicine · JPSaiseikai Utsunomiya hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cilnidipine (Cil), which is an L-/N-type calcium channel blocker (CCB), has been known to provide renal protection by decreasing the activity of the sympathetic nervous system (SNS) and the renin-angiotensin system. In this study, we compared the effects of the combination of Cil and amlodipine (Aml), which is an L-type CCB, with an angiotensin (Ang) II receptor blocker on diabetic cardiorenal damage in spontaneously type 2 diabetic rats. Seventeen-week-old Otsuka Long-Evans Tokushima Fatty rats were randomly assigned to receive Cil, Aml, valsartan (Val), Cil + Val, Aml + Val, or a vehicle (eight rats per group) for 22 weeks. Antihypertensive potencies were nearly equal among the CCB monotherapy groups and the combination therapy groups. The lowering of blood pressure by either treatment did not significantly affect the glycemic variables. However, exacerbations of renal and heart failure were significantly suppressed in rats administered Cil or Val, and additional suppression was observed in those administered Cil + Val. Although Val increased the renin-Ang system, Aml + Val treatment resulted in additional increases in these parameters, while Cil + Val did not show such effects. Furthermore, Cil increased the ratio of Ang-(1-7) to Ang-I, despite the fact that Val and Aml + Val decreased the Ang-(1-7) levels. These actions of Cil + Val might be due to their synergistic inhibitory effect on the activity of the SNS, and on aldosterone secretion through N-type calcium channel antagonism and Ang II receptor type 1 antagonism. Thus, Cil may inhibit the progression of cardiorenal disease in type 2 diabetes patients by acting as an N-type CCB and inhibiting the aldosterone secretion and SNS activation when these drugs were administered in combination with an Ang II receptor blocker.

Indexed as

Angiotensin II Type 1 Receptor BlockersAnimalsCalcium Channel BlockersCalcium Channels, L-TypeCalcium Channels, N-TypeCardio-Renal SyndromeDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2DihydropyridinesMaleRatsRats, Inbred OLETFAngiotensin II Type 1 Receptor BlockersCalcium Channel BlockersCalcium Channels, L-TypeCalcium Channels, N-TypecilnidipineDihydropyridinesangiotensincalcium channel blockercombination therapytype 2 diabetes mellitus

Identifiers

PMID24970998
PMCPMC4069052
OpenAlexW2017776654

What OpenQuestion holds

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LicenceCC BY-NC
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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.