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Published on: February 10, 2013
Testosterone negatively regulates right ventricular load stress responses in mice
Anna R Hemnes1, Karen B Maynard, Hunter C Champion
1Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Pulmonary Circulation
|November 7, 2012
Summary
Testosterone influences right ventricular (RV) hypertrophy and fibrosis in response to pulmonary arterial hypertension (PAH) load stress. While testosterone deprivation improved survival in mice with PAH, its direct impact on RV hemodynamics was minimal.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Pulmonary Hypertension Research
Background:
- Right ventricular (RV) function is critical in pulmonary arterial hypertension (PAH) mortality.
- Male sex is a significant predictor of mortality in PAH.
- The impact of testosterone on RV structure and function under load stress remains unclear.
Purpose of the Study:
- To investigate the effects of testosterone levels on RV hypertrophic responses.
- To determine testosterone's influence on RV fibrosis and overall function.
- To assess testosterone's role in RV adaptation to pulmonary artery banding (PAB) induced load stress.
Main Methods:
- Male C57BL/6 mice underwent castration or sham procedures.
- Pulmonary artery banding (PAB) or sham surgery was performed to induce load stress.
- Testosterone pellets were administered to a subset of castrated mice; hemodynamic measurements and tissue harvesting were conducted.
Main Results:
- Castration reduced RV hypertrophy (RV/LV+S ratio, myocyte diameter) in PAB mice.
- Testosterone replacement normalized these hypertrophic parameters but increased RV fibrosis.
- Testosterone deprivation improved survival in PAB mice, with minimal effects on RV hemodynamics.
Conclusions:
- Testosterone modulates RV hypertrophic response to load stress via myocyte size and fibrosis.
- Testosterone deprivation enhances survival in a mouse model of PAH.
- Further research is needed to elucidate testosterone's role in RV dysfunction for human PAH.
