Skip to main content
  • American Heart Association
  • Science Volunteer
  • Warning Signs
  • Advanced Search
  • Donate

  • Home
  • About this Journal
    • General Statistics
    • Editorial Board
    • Editors
    • Information for Advertisers
    • Author Reprints
    • Commercial Reprints
    • Customer Service and Ordering Information
  • All Issues
  • Subjects
    • All Subjects
    • Arrhythmia and Electrophysiology
    • Basic, Translational, and Clinical Research
    • Critical Care and Resuscitation
    • Epidemiology, Lifestyle, and Prevention
    • Genetics
    • Heart Failure and Cardiac Disease
    • Hypertension
    • Imaging and Diagnostic Testing
    • Intervention, Surgery, Transplantation
    • Quality and Outcomes
    • Stroke
    • Vascular Disease
  • Browse Features
    • AHA Guidelines and Statements
    • Acknowledgment of Reviewers
    • Clinical Implications
    • Clinical-Pathological Conferences
    • Controversies in Hypertension
    • Editors' Picks
    • Guidelines Debate
    • Meeting Abstracts
    • Recent Advances in Hypertension
    • SPRINT Trial: the Conversation Continues
  • Resources
    • Instructions to Reviewers
    • Instructions for Authors
    • →Article Types
    • → Submission Guidelines
      • Research Guidelines
        • Minimum Information About Microarray Data Experiments (MIAME)
      • Abstract
      • Acknowledgments
      • Clinical Implications (Only by invitation)
      • Conflict(s) of Interest/Disclosure(s) Statement
      • Figure Legends
      • Figures
      • Novelty and Significance: 1) What Is New, 2) What Is Relevant?
      • References
      • Sources of Funding
      • Tables
      • Text
      • Title Page
      • Online/Data Supplement
    • →Tips for Easier Manuscript Submission
    • → General Instructions for Revised Manuscripts
      • Change of Authorship Form
    • → Costs to Authors
    • → Open Access, Repositories, & Author Rights Q&A
    • Permissions to Reprint Figures and Tables
    • Journal Policies
    • Scientific Councils
    • AHA Journals RSS Feeds
    • International Users
    • AHA Newsroom
  • AHA Journals
    • AHA Journals Home
    • Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)
    • Circulation
    • → Circ: Arrhythmia and Electrophysiology
    • → Circ: Genomic and Precision Medicine
    • → Circ: Cardiovascular Imaging
    • → Circ: Cardiovascular Interventions
    • → Circ: Cardiovascular Quality & Outcomes
    • → Circ: Heart Failure
    • Circulation Research
    • Hypertension
    • Stroke
    • Journal of the American Heart Association
  • Facebook
  • Twitter

  • My alerts
  • Sign In
  • Join

  • Advanced search

Header Publisher Menu

  • American Heart Association
  • Science Volunteer
  • Warning Signs
  • Advanced Search
  • Donate

Hypertension

  • My alerts
  • Sign In
  • Join

  • Facebook
  • Twitter
  • Home
  • About this Journal
    • General Statistics
    • Editorial Board
    • Editors
    • Information for Advertisers
    • Author Reprints
    • Commercial Reprints
    • Customer Service and Ordering Information
  • All Issues
  • Subjects
    • All Subjects
    • Arrhythmia and Electrophysiology
    • Basic, Translational, and Clinical Research
    • Critical Care and Resuscitation
    • Epidemiology, Lifestyle, and Prevention
    • Genetics
    • Heart Failure and Cardiac Disease
    • Hypertension
    • Imaging and Diagnostic Testing
    • Intervention, Surgery, Transplantation
    • Quality and Outcomes
    • Stroke
    • Vascular Disease
  • Browse Features
    • AHA Guidelines and Statements
    • Acknowledgment of Reviewers
    • Clinical Implications
    • Clinical-Pathological Conferences
    • Controversies in Hypertension
    • Editors' Picks
    • Guidelines Debate
    • Meeting Abstracts
    • Recent Advances in Hypertension
    • SPRINT Trial: the Conversation Continues
  • Resources
    • Instructions to Reviewers
    • Instructions for Authors
    • →Article Types
    • → Submission Guidelines
    • →Tips for Easier Manuscript Submission
    • → General Instructions for Revised Manuscripts
    • → Costs to Authors
    • → Open Access, Repositories, & Author Rights Q&A
    • Permissions to Reprint Figures and Tables
    • Journal Policies
    • Scientific Councils
    • AHA Journals RSS Feeds
    • International Users
    • AHA Newsroom
  • AHA Journals
    • AHA Journals Home
    • Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)
    • Circulation
    • → Circ: Arrhythmia and Electrophysiology
    • → Circ: Genomic and Precision Medicine
    • → Circ: Cardiovascular Imaging
    • → Circ: Cardiovascular Interventions
    • → Circ: Cardiovascular Quality & Outcomes
    • → Circ: Heart Failure
    • Circulation Research
    • Hypertension
    • Stroke
    • Journal of the American Heart Association
Original Article

Small-Conductance Ca2+-Activated Potassium Channels Negatively Regulate Aldosterone Secretion in Human Adrenocortical Cells

Tingting Yang, Hai-Liang Zhang, Qingnan Liang, Yingtang Shi, Yan-Ai Mei, Paula Q. Barrett, Changlong Hu
Download PDF
https://doi.org/10.1161/HYPERTENSIONAHA.116.07094
Hypertension. 2016;HYPERTENSIONAHA.116.07094
Originally published July 18, 2016
Tingting Yang
From the Department of Physiology and Biophysics, School of Life Sciences, Institutes of Brain Science (T.Y., Q.L., Y.-A.M., C.H.) and Department of Oncology, Shanghai Medical College (H.-L.Z.), Fudan University, China; Department of Urology, Fudan University Shanghai Cancer Center, China (H.-L.Z.); and Department of Pharmacology, University of Virginia, Charlottesville (Y.S., P.Q.B.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Hai-Liang Zhang
From the Department of Physiology and Biophysics, School of Life Sciences, Institutes of Brain Science (T.Y., Q.L., Y.-A.M., C.H.) and Department of Oncology, Shanghai Medical College (H.-L.Z.), Fudan University, China; Department of Urology, Fudan University Shanghai Cancer Center, China (H.-L.Z.); and Department of Pharmacology, University of Virginia, Charlottesville (Y.S., P.Q.B.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Qingnan Liang
From the Department of Physiology and Biophysics, School of Life Sciences, Institutes of Brain Science (T.Y., Q.L., Y.-A.M., C.H.) and Department of Oncology, Shanghai Medical College (H.-L.Z.), Fudan University, China; Department of Urology, Fudan University Shanghai Cancer Center, China (H.-L.Z.); and Department of Pharmacology, University of Virginia, Charlottesville (Y.S., P.Q.B.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yingtang Shi
From the Department of Physiology and Biophysics, School of Life Sciences, Institutes of Brain Science (T.Y., Q.L., Y.-A.M., C.H.) and Department of Oncology, Shanghai Medical College (H.-L.Z.), Fudan University, China; Department of Urology, Fudan University Shanghai Cancer Center, China (H.-L.Z.); and Department of Pharmacology, University of Virginia, Charlottesville (Y.S., P.Q.B.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yan-Ai Mei
From the Department of Physiology and Biophysics, School of Life Sciences, Institutes of Brain Science (T.Y., Q.L., Y.-A.M., C.H.) and Department of Oncology, Shanghai Medical College (H.-L.Z.), Fudan University, China; Department of Urology, Fudan University Shanghai Cancer Center, China (H.-L.Z.); and Department of Pharmacology, University of Virginia, Charlottesville (Y.S., P.Q.B.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Paula Q. Barrett
From the Department of Physiology and Biophysics, School of Life Sciences, Institutes of Brain Science (T.Y., Q.L., Y.-A.M., C.H.) and Department of Oncology, Shanghai Medical College (H.-L.Z.), Fudan University, China; Department of Urology, Fudan University Shanghai Cancer Center, China (H.-L.Z.); and Department of Pharmacology, University of Virginia, Charlottesville (Y.S., P.Q.B.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Changlong Hu
From the Department of Physiology and Biophysics, School of Life Sciences, Institutes of Brain Science (T.Y., Q.L., Y.-A.M., C.H.) and Department of Oncology, Shanghai Medical College (H.-L.Z.), Fudan University, China; Department of Urology, Fudan University Shanghai Cancer Center, China (H.-L.Z.); and Department of Pharmacology, University of Virginia, Charlottesville (Y.S., P.Q.B.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Supplemental Materials
  • Info & Metrics
  • eLetters

Jump to

  • Article
  • Supplemental Materials
  • Info & Metrics
  • eLetters
Loading

Abstract

Aldosterone, which plays a key role in maintaining water and electrolyte balance, is produced by zona glomerulosa cells of the adrenal cortex. Autonomous overproduction of aldosterone from zona glomerulosa cells causes primary hyperaldosteronism. Recent clinical studies have highlighted the pathological role of the KCNJ5 potassium channel in primary hyperaldosteronism. Our objective was to determine whether small-conductance Ca2+-activated potassium (SK) channels may also regulate aldosterone secretion in human adrenocortical cells. We found that apamin, the prototypic inhibitor of SK channels, decreased membrane voltage, raised intracellular Ca2+ and dose dependently increased aldosterone secretion from human adrenocortical H295R cells. By contrast, 1-Ethyl-2-benzimidazolinone, an agonist of SK channels, antagonized apamin’s action and decreased aldosterone secretion. Commensurate with an increase in aldosterone production, apamin increased mRNA expression of steroidogenic acute regulatory protein and aldosterone synthase that control the early and late rate-limiting steps in aldosterone biosynthesis, respectively. In addition, apamin increased angiotensin II–stimulated aldosterone secretion, whereas 1-Ethyl-2-benzimidazolinone suppressed both angiotensin II– and high K+–stimulated production of aldosterone in H295R cells. These findings were supported by apamin-modulation of basal and angiotensin II–stimulated aldosterone secretion from acutely prepared slices of human adrenals. We conclude that SK channel activity negatively regulates aldosterone secretion in human adrenocortical cells. Genetic association studies are necessary to determine whether mutations in SK channel subtype 2 genes may also drive aldosterone excess in primary hyperaldosteronism.

  • adrenal cortex
  • aldosterone secretion
  • angiotensin II
  • apamin
  • hyperaldosteronism
  • small-conductance Ca2+-activated potassium channels
  • Received January 5, 2016.
  • Revision received January 18, 2016.
  • Accepted May 5, 2016.
  • © 2016 American Heart Association, Inc.
Back to top
Next Article

Current Issue

Hypertension
May 2018, Volume 71, Issue 5
  • Table of Contents
Next Article

Jump to

  • Article
  • Supplemental Materials
  • Info & Metrics
  • eLetters

Article Tools

  • Print
  • Citation Tools
    Small-Conductance Ca2+-Activated Potassium Channels Negatively Regulate Aldosterone Secretion in Human Adrenocortical Cells
    Tingting Yang, Hai-Liang Zhang, Qingnan Liang, Yingtang Shi, Yan-Ai Mei, Paula Q. Barrett and Changlong Hu
    Hypertension. 2016;HYPERTENSIONAHA.116.07094, originally published July 18, 2016
    https://doi.org/10.1161/HYPERTENSIONAHA.116.07094

    Citation Manager Formats

    • BibTeX
    • Bookends
    • EasyBib
    • EndNote (tagged)
    • EndNote 8 (xml)
    • Medlars
    • Mendeley
    • Papers
    • RefWorks Tagged
    • Ref Manager
    • RIS
    • Zotero
  • Article Alerts
    Log in to Email Alerts with your email address.
  • Save to my folders

Share this Article

  • Email

    Thank you for your interest in spreading the word on Hypertension.

    NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

    Enter multiple addresses on separate lines or separate them with commas.
    Small-Conductance Ca2+-Activated Potassium Channels Negatively Regulate Aldosterone Secretion in Human Adrenocortical Cells
    (Your Name) has sent you a message from Hypertension
    (Your Name) thought you would like to see the Hypertension web site.
  • Share on Social Media
    Small-Conductance Ca2+-Activated Potassium Channels Negatively Regulate Aldosterone Secretion in Human Adrenocortical Cells
    Tingting Yang, Hai-Liang Zhang, Qingnan Liang, Yingtang Shi, Yan-Ai Mei, Paula Q. Barrett and Changlong Hu
    Hypertension. 2016;HYPERTENSIONAHA.116.07094, originally published July 18, 2016
    https://doi.org/10.1161/HYPERTENSIONAHA.116.07094
    del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo

Related Articles

Cited By...

Subjects

  • Cardiology
    • Etiology
      • Hypertension
        • Hypertension
  • Arrhythmia and Electrophysiology
    • Electrophysiology
  • Basic, Translational, and Clinical Research
    • Ion Channels/Membrane Transport
    • Basic Science Research
    • ACE/Angiotensin Receptors/Renin Angiotensin System

Hypertension

  • About Hypertension
  • Instructions for Authors
  • AHA CME
  • Guidelines and Statements
  • Permissions
  • Journal Policies
  • Email Alerts
  • Open Access Information
  • AHA Journals RSS
  • AHA Newsroom

Editorial Office Address:
7272 Greenville Ave.
Dallas, TX 75231
email: hypertension@heart.org

Information for:
  • Advertisers
  • Subscribers
  • Subscriber Help
  • Institutions / Librarians
  • Institutional Subscriptions FAQ
  • International Users
American Heart Association Learn and Live
National Center
7272 Greenville Ave.
Dallas, TX 75231

Customer Service

  • 1-800-AHA-USA-1
  • 1-800-242-8721
  • Local Info
  • Contact Us

About Us

Our mission is to build healthier lives, free of cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question. Find Out More about the American Heart Association

  • Careers
  • SHOP
  • Latest Heart and Stroke News
  • AHA/ASA Media Newsroom

Our Sites

  • American Heart Association
  • American Stroke Association
  • For Professionals
  • More Sites

Take Action

  • Advocate
  • Donate
  • Planned Giving
  • Volunteer

Online Communities

  • AFib Support
  • Garden Community
  • Patient Support Network
  • Professional Online Network

Follow Us:

  • Follow Circulation on Twitter
  • Visit Circulation on Facebook
  • Follow Circulation on Google Plus
  • Follow Circulation on Instagram
  • Follow Circulation on Pinterest
  • Follow Circulation on YouTube
  • Rss Feeds
  • Privacy Policy
  • Copyright
  • Ethics Policy
  • Conflict of Interest Policy
  • Linking Policy
  • Diversity
  • Careers

©2018 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. The American Heart Association is a qualified 501(c)(3) tax-exempt organization.
*Red Dress™ DHHS, Go Red™ AHA; National Wear Red Day ® is a registered trademark.

  • PUTTING PATIENTS FIRST National Health Council Standards of Excellence Certification Program
  • BBB Accredited Charity
  • Comodo Secured