Modulation of hypertensive heart disease by estrogen

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Published on: August 13, 2019

C Grohé1, S Kahlert, K Löbbert

  • 1Medizinische Universitäts-Poliklinik, University of Bonn, Germany.

Steroids
|April 1, 1996
PubMed

Insights

Estrogen metabolites stimulate cardiac fibroblast growth and affect calcium channels in heart cells. These findings help explain gender and age differences in hypertensive heart disease.

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Molecular Cardiology

Background:

  • Left ventricular hypertrophy (LVH) is a risk factor for morbidity and mortality in hypertensive heart disease.
  • Gender-based differences exist in cardiac hypertrophy, with higher mortality in men.
  • The role of estrogen in cardiac hypertrophy pathogenesis is not well understood.

Purpose of the Study:

  • Investigate the influence of estrogen metabolites on cardiac fibroblast growth.
  • Examine the effect of estrogen metabolites on immediate early gene c-Fos expression.
  • Determine estrogen's impact on the L-type calcium channel in cardiomyocytes.

Main Methods:

  • Incubated neonatal rat cardiac fibroblasts with various estrogen metabolites.
  • Measured bromodeoxyuridine incorporation to assess fibroblast growth.
  • Assessed L-type calcium channel currents in adult guinea pig cardiomyocytes using whole-cell patch clamp.

Main Results:

  • Estrogen metabolites stimulated cardiac fibroblast growth, with 2-hydroxyestrone being the most potent.
  • 17 beta-estradiol significantly reduced L-type calcium channel current in cardiomyocytes by approximately 20%.

Conclusions:

  • Estrogen exerts both short-term (non-genomic) and long-term (genomic) effects on the heart.
  • These estrogen-mediated effects may contribute to gender- and age-based disparities in hypertensive heart disease.
Abstract

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