Evidence map›Paper›PMID 22689262›Full record

ReviewEndocrinology2012

Minireview: aldosterone biosynthesis: electrically gated for our protection.

Nick A Guagliardo, Junlan Yao, Changlong Hu, Paula Q Barrett

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 46 citations in OpenAlex.

  1. Channelopathy linkingJCEM case reports · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Channels and pumps in aldosterone-producing adenomas.The Journal of clinical endocrinology and metabolism · 2014
    Article
  16. Overview of the genetic determinants of primary aldosteronism.The application of clinical genetics · 2014
    Review
  17. Review
  18. Regulation of aldosterone biosynthesis by the Kir3.4 (KCNJ5) potassium channel.Clinical and experimental pharmacology & physiology · 2013
    Review
  19. Review
  20. 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

4 authors at 2 institutions in 2 countries.

Nick A GuagliardoDepartment of Pharmacology, University of Virginia, P.O. Box 800735, Jordan Hall 5th Floor, 5058, Charlottesville, Virginia 22908, USA.
Junlan Yao
Changlong Hu
Paula Q Barrett
University of Virginia · USFudan University · CN

Funding

T TYPE CALCIUM CHANNELS AND ALDOSTERONE SECRETIONR01HL036977 · NHLBI · YALE UNIVERSITY · PI BARRETT, PAULA Q · 1987 to 2013
$4.2M
Two-Pore Domain Potassium Channels and Aldosterone SecretionR01HL089717 · NHLBI · UNIVERSITY OF VIRGINIA · PI BARRETT, PAULA Q, BAYLISS, DOUGLAS A. · 2008 to 2017
$3.4M
NHLBI NIH HHS HL-036977NHLBI NIH HHS HL-089717NHLBI NIH HHS R01 HL036977NHLBI NIH HHS R01 HL089717
6 · The paper itself

Abstract

Aldosterone produced by adrenal zona glomerulosa (ZG) cells plays an important role in maintaining salt/water balance and, hence, blood pressure homeostasis. However, when dysregulated, aldosterone advances renal and cardiovascular disease states. Multiple steps in the steroidogenic pathway require Ca(2+), and the sustained production of aldosterone depends on maintained Ca(2+) entry into the ZG cell. Nevertheless, the recorded membrane potential of isolated ZG cells is extremely hyperpolarized, allowing the opening of only a small fraction of low-voltage-activated Ca(2+) channels of the Ca(v)3.x family, the major Ca(2+) conductance on the ZG cell membrane. As a consequence, to activate sufficient Ca(2+) channels to sustain the production of aldosterone, aldosterone secretagogs would be required to affect large decreases in membrane voltage, a requirement that is inconsistent with the exquisite sensitivity of aldosterone production in vivo to small changes (0.1 mm) in extracellular K(+). In this review, we evaluate the contribution of membrane voltage and voltage-dependent Ca(2+) channels to the control of aldosterone production and consider data highlighting the electrical excitability of the ZG cell. This intrinsic capacity of ZG cells to behave as electrical oscillators provides a platform from which to generate a recurring Ca(2+) signal that is compatible with the lengthy time course of steroidogenesis and provides an alternative model for the physiological regulation of aldosterone production that permits both amplitude and temporal modulation of the Ca(2+) signal.

Indexed as

AldosteroneAnimalsCalciumCalcium ChannelsHumansZona GlomerulosaAldosteroneCalciumCalcium Channels

Identifiers

PMID22689262
PMCPMC3404360
OpenAlexW2000644153

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.