Zusammenfassung
Background/Aims: The role of endothelin ( ET) in cardiovascular remodeling was investigated by treating uninephrectomized spontaneously hypertensive rats of the stroke-prone strain ( UNX-SHRsp) on normal- or high (3%)-salt diet with the selective ET A receptor blocker LU 135252. Methods: SHRsp on normal or high salt were sham-operated ( n = 10/ 11) or UNX; UNX received no treatment ( n = 10/ 15) ...
Zusammenfassung
Background/Aims: The role of endothelin ( ET) in cardiovascular remodeling was investigated by treating uninephrectomized spontaneously hypertensive rats of the stroke-prone strain ( UNX-SHRsp) on normal- or high (3%)-salt diet with the selective ET A receptor blocker LU 135252. Methods: SHRsp on normal or high salt were sham-operated ( n = 10/ 11) or UNX; UNX received no treatment ( n = 10/ 15) or 100 mg/ kg body weight LU 135252 ( n = 10/ 10). Systolic blood pressure ( BP) was measured weekly. After perfusion fixation the heart and the aorta were analyzed using quantitative morphological and stereological techniques. Results: No effect was seen in normal- salt groups. In high-salt animals UNX caused left ventricular (LV) hypertrophy which was prevented by LU 135252 ( p < 0.001). LU 135252 only lowered BP during the last 2 weeks of the 12-week experiment. UNX showed hypertrophic remodeling of intramyocardial arterioles. Treatment with LU 135252 caused lower wall: lumen ratio and wall thickness of LV intramyocardial arterioles ( p < 0.01). In the descending thoracic aorta UNX caused thickening of the media. The media area and the wall: lumen ratio were lower in UNX + LU 135252 as compared to untreated UNX ( p < 0.01 and p < 0.05, respectively). Conclusion: In SHRsp UNX causes hypertrophic cardiovascular remodeling only in the presence of salt loading. These effects are largely BP-independent and prevented by ET A receptor blockade.
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