Evidence map›Paper›PMID 27515419›Full record

ArticleBioscience reports2016

On the top of ARB N/L type Ca channel blocker leads to less elevation of aldosterone.

Tadashi Konoshita, Saori Kaeriyama, Machi Urabe, Takahiro Nakaya, Mika Yamada, Mai Ichikawa, Katsushi Yamamoto, Satsuki Sato, Michiko Imagawa, Miki Fujii and 7 more

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 86% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

17 authors at 2 institutions in 1 country.

Tadashi KonoshitaThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan konosita@u-fukui.ac.jp.
Saori KaeriyamaThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Machi UrabeThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Takahiro NakayaThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Mika YamadaThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Mai IchikawaThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Katsushi YamamotoThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Satsuki SatoThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Michiko ImagawaThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Miki FujiiThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Yasukazu MakinoThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Yasuo ZenimaruThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Shigeyuki WakaharaThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Jinya SuzukiThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Tamotsu IshizukaThird Department of Internal Medicine, University of Fukui Faculty of Medical Sciences, Fukui, Japan.
Hiroyuki NakamuraDepartment of Environmental and Preventive Medicine, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Genomic Disease Outcome Consortium (G-DOC) Study Investigators
University of Fukui · JPKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activation of the renin-angiotensin system (RAS) is one of the unfavourable characteristics of calcium channel blocker (CCB). N type calcium channel is thought to be involved in renin gene transcription and adrenal aldosterone release. Accordingly, N/L type CCB has a possibility of less elevation of plasma aldosterone concentrations (PAC) among CCBs. In a monotherapy study, we had already demonstrated that N/L type CCB leads to less activation of the RAS compared with L type CCB. The objective of this study is to substantiate the hypothesis that at the condition of additive administration on the top of an angiotensin receptor blocker (ARB), still N/L type CCB leads to less elevation of PAC compared with L type one. Subjects were 60 hypertensives administered with valsartan. As an open label study, amlodipine (L type) or cilnidipine (N/L type) were administered on the top of valsartan (ARB) in a cross-over manner. Results were as follows (valsartan+amlodipine compared with valsartan+cilnidipine): systolic blood pressure (SBP)/diastolic blood pressure (DBP) (mmHg): 132±10/76±10 compared with 131±10/77±9, P=0.95/0.48, plasma renin activity (PRA) (ng/ml·h): 2.41±2.67 compared with 2.00±1.50 P=0.20, PAC (pg/ml): 77.3±31.0 compared with 67.4±24.8, P<0.05, urinary albumin excretion (UAE) (mg/gCr): 105.9±216.1 compared with 73.9±122.2, P<0.05. Thus, PAC at cilnidipine was significantly lower than those at amlodipine in spite of the comparable BP reductions. Besides, UAE was significantly lower at cilnidipine. In conclusion, on the top of the ARB, it is suggested that cilnidipine administration might lead to less elevation of PAC and reduction in UAE compared with amlodipine.

Indexed as

AgedAldosteroneAmlodipineAngiotensin Receptor AntagonistsBlood PressureCalcium Channel BlockersCalcium Channels, L-TypeCalcium Channels, N-TypeDihydropyridinesDrug CombinationsFemaleHumansHypertensionMaleMiddle AgedRenin-Angiotensin SystemAldosteroneAmlodipineAngiotensin Receptor AntagonistsCalcium Channel BlockersCalcium Channels, L-TypeCalcium Channels, N-TypecilnidipineDihydropyridinesDrug CombinationsValsartanaldosteroneamlodipineangiotensin receptor blockercalcium channel blockercilnidipinereninrenin–angiotensin system

Identifiers

PMID27515419
PMCPMC5025805
OpenAlexW2517031042

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.