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Right Ventricular Hypertrophy in Spontaneously Hypertensive Rats (SHR/NHsd) Is Associated with Inter-Individual
Alicia Langer1, Rolf Schreckenberg1, Klaus-Dieter Schlüter1
1Physiologisches Institut, Justus-Liebig University, Aulweg 129, D-35392 Giessen, Germany.
Biology
|October 25, 2024
Summary
Spontaneously hypertensive rats can develop right ventricular hypertrophy due to decreased lung endothelin-B receptor expression. This molecular change increases lung vascular resistance, leading to right ventricular hypertrophy in a subset of rats.
Area of Science:
- Cardiovascular Research
- Pulmonary Hypertension
- Genetics
Background:
- Spontaneously hypertensive rats (SHRs) commonly exhibit left ventricular hypertrophy.
- The development of right ventricular hypertrophy in SHRs is not well-characterized.
- A genetic variant may underlie right ventricular hypertrophy in a subpopulation of SHRs.
Purpose of the Study:
- To investigate the incidence and molecular mechanisms of right ventricular hypertrophy in SHRs.
- To compare the molecular profiles of the lung and right ventricle in rats with and without right ventricular hypertrophy.
- To identify potential genetic factors contributing to right ventricular hypertrophy in SHRs.
Main Methods:
- Analysis of 76 female SHR/NHsd rats, categorizing them into groups with and without right ventricular hypertrophy.
- Molecular analysis of lung and right ventricle tissues, focusing on endothelin receptor expression and related proteins.
- Comparison of molecular fingerprints between hypertensive rats with right ventricular hypertrophy, hypertensive rats without right ventricular hypertrophy, and normotensive controls.
Main Results:
- Severe right ventricular hypertrophy (SHR-RVH) was observed in 7% of analyzed SHRs.
- SHR-RVH did not correlate with rat age and was present pre-hypertension in one case.
- SHR-RVH was associated with decreased lung endothelin-B receptor (EDNRB) expression, increased lung endothelin-1, and increased ACTA2A expression.
- Down-regulation of the endothelin-A receptor (EDNRA) was noted in the right ventricle of SHR-RVH rats.
Conclusions:
- Reduced expression of the endothelin-B receptor in the lung may trigger increased pulmonary vascular resistance, leading to right ventricular hypertrophy in susceptible SHRs.
- This study identifies a potential genetic variant associated with right ventricular hypertrophy in a defined SHR strain.
- The findings provide novel insights into the pathophysiology of right ventricular hypertrophy in the context of hypertension.
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