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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Impact of dihydrotestosterone on L-type calcium channels in human ventricular cardiomyocytes

Fikret Er1, Natig Gassanov, Mathias C Brandt

  • 1Department of Internal Medicine III, University of Cologne, 50937 Cologne, Germany.

Endocrine Research
|August 25, 2009
PubMed

Insights

Dihydrotestosterone increases calcium current in human heart cells by upregulating Ca(V)1.2 channels. This finding may explain cardiovascular effects seen in androgenic steroid abuse.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Endocrinology

Background:

  • Testosterone's cardiovascular effects are debated, with evidence for direct cardiac actions.
  • The impact of testosterone on human cardiac L-type calcium channels is unknown.
  • L-type calcium channels are crucial for cardiac electro-mechanical coupling.

Purpose of the Study:

  • To investigate the effect of dihydrotestosterone on human cardiac L-type calcium channels.
  • To determine if dihydrotestosterone influences the expression of Ca(V)1.2 subunits.

Main Methods:

  • Human ventricular myocytes were isolated from heart transplant patients.
  • Whole-cell patch-clamp electrophysiology was used to measure L-type calcium current (I(Ca,L)).
  • Dihydrotestosterone treatment was applied to cultured cardiomyocytes.

Main Results:

  • Dihydrotestosterone (100 nmol/L for 24-30h) significantly increased I(Ca,L) density in human ventricular myocytes.
  • The current-voltage relationship of I(Ca,L) remained unchanged.
  • Dihydrotestosterone treatment led to a 1.35-fold increase in Ca(V)1.2 subunit expression.

Conclusions:

  • Dihydrotestosterone enhances L-type calcium current density in human ventricular myocytes.
  • This effect is mediated by the upregulation of the Ca(V)1.2 channel subunit.
  • These findings offer a potential mechanism for the cardiovascular effects associated with androgenic steroid abuse.
Abstract

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