Evidence map›Paper›PMID 27098837›Full record

ArticleScientific reports2016

Regulation of aldosterone secretion by Cav1.3.

Catherine B Xie, Lalarukh Haris Shaikh, Sumedha Garg, Gizem Tanriver, Ada E D Teo, Junhua Zhou, Carmela Maniero, Wanfeng Zhao, Soosung Kang, Richard B Silverman and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Evaluation of Aldosterone Suppression by Cinnarizine, a Putative Cav1.3 Inhibitor.The Journal of clinical endocrinology and metabolism · 2025
    Trial
  2. Article
  3. SomaticHypertension (Dallas, Tex. : 1979) · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. CaBritish journal of pharmacology · 2023
    Review
  9. CACNA1D-Related Channelopathies: From Hypertension to Autism.Handbook of experimental pharmacology · 2023
    Review
  10. Clinical Translationality ofInternational journal of molecular sciences · 2022
    Review
  11. The Involvement of CaFrontiers in neural circuits · 2021
    Article
  12. The Potential Role of Aldosterone-Producing Cell Clusters in Adrenal Disease.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2020
    Review
  13. Article
  14. Molecular Mechanisms of Primary Aldosteronism.Endocrinology and metabolism (Seoul, Korea) · 2019
    Review
  15. Article
  16. Article
  17. Review
  18. Targeted Molecular Characterization of Aldosterone-Producing Adenomas in White Americans.The Journal of clinical endocrinology and metabolism · 2018
    Article
  19. Cellular and Genetic Causes of Idiopathic Hyperaldosteronism.Hypertension (Dallas, Tex. : 1979) · 2018
    Article
  20. Aging and Adrenal Aldosterone Production.Hypertension (Dallas, Tex. : 1979) · 2018
    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

12 authors at 5 institutions in 3 countries.

Catherine B XieClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Lalarukh Haris ShaikhClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Sumedha GargClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Gizem TanriverClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Ada E D TeoClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Junhua ZhouClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Carmela ManieroClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Wanfeng ZhaoHuman Research Tissue Bank, Cambridge University Hospitals NHS Foundation Trust, Addenbrooke's Hospital, Cambridge, CB2 0QQ, UK.
Soosung KangDepartment of Chemistry, Chemistry of Life Processes Institute, and Center for Molecular Innovation and Drug Discovery, Northwestern University, Evanston, Illinois 60208-3113, USA.
Richard B SilvermanDepartment of Chemistry, Chemistry of Life Processes Institute, and Center for Molecular Innovation and Drug Discovery, Northwestern University, Evanston, Illinois 60208-3113, USA.
Elena A B AzizanClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Morris J BrownClinical Pharmacology Unit, University of Cambridge, Box 110, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Addenbrooke's Hospital · GBUniversity of Cambridge · GBNorthwestern University · USWilliam Harvey Research Institute · GBYale University · US

Funding

British Heart Foundation FS/11/35/28871British Heart Foundation FS/14/12/30540British Heart Foundation FS/14/75/31134Wellcome TrustWellcome Trust 085686/Z/08/A
6 · The paper itself

Abstract

Aldosterone-producing adenomas (APAs) vary in phenotype and genotype. Zona glomerulosa (ZG)-like APAs frequently have mutations of an L-type calcium channel (LTCC) CaV1.3. Using a novel antagonist of CaV1.3, compound 8, we investigated the role of CaV1.3 on steroidogenesis in the human adrenocortical cell line, H295R, and in primary human adrenal cells. This investigational drug was compared with the common antihypertensive drug nifedipine, which has 4.5-fold selectivity for the vascular LTCC, CaV1.2, over CaV1.3. In H295R cells transfected with wild-type or mutant CaV1.3 channels, the latter produced more aldosterone than wild-type, which was ameliorated by 100 μM of compound 8. In primary adrenal and non-transfected H295R cells, compound 8 decreased aldosterone production similar to high concentration of nifedipine (100 μM). Selective CaV1.3 blockade may offer a novel way of treating primary hyperaldosteronism, which avoids the vascular side effects of CaV1.2-blockade, and provides targeted treatment for ZG-like APAs with mutations of CaV1.3.

Indexed as

AldosteroneCalcium Channel BlockersCalcium Channels, L-TypeCell LineCells, CulturedGenotypeHumansMutationNifedipineProtein TransportAldosteroneCACNA1D protein, humanCalcium Channel BlockersCalcium Channels, L-TypeNifedipine

Identifiers

PMID27098837
PMCPMC4876952
OpenAlexW2339300299

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.