Cardiac remodeling and function following exercise and angiotensin II receptor antagonism

被引:7
|
作者
Libonati, Joseph R. [1 ]
机构
[1] Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA
关键词
Training; Systolic function; Diastole; Heart; Losartan; Hypertrophy; STRETCH-INDUCED HYPERTROPHY; MYOCYTES IN-VITRO; MYOCARDIAL-INFARCTION; TYPE-1; RECEPTOR; RATS; LOSARTAN; HYPERTENSION; STRESS; HEART; RESPONSIVENESS;
D O I
10.1007/s00421-011-2263-y
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The purpose of this study was to test the impact of chronic exercise training combined with selective angiotensin II receptor (AT1) antagonism on systolic blood pressure (SBP) and the left-ventricular pressure-volume relationship in normotensive, non-infarcted rat hearts. Wistar rats (N = 19) were randomly assigned to either a sedentary control group (N = 8) or an exercise-trained group (N = 11). Losartan was administered to individually caged rats via the drinking water (10 mg/kg/d). Exercise training consisted of running on a motorized driven treadmill for 6 weeks at 30 m/min, 60 min/day, 5 days/week. Tail cuff SBP was measured weekly. Left ventricular performance was assessed in an ex vivo Langendorff isovolumic mode. One week of losartan treatment significantly reduced SBP in both groups by 13% relative to baseline (P < 0.05). SBP was lower in exercise-trained animals versus sedentary animals in the later weeks of the protocol (P < 0.05) Body weight was significantly lower in exercise-trained animals versus sedentary animals, but heart weight, heart to body weight ratio, atrial weight, and absolute left ventricular mass and length were similar between groups. The LV systolic pressure-volume relationship (PV) and systolic elastance were significantly greater in exercise-trained animals versus sedentary controls (P < 0.05). The left ventricular end-diastolic PV and diastolic stiffness were similar between exercise-trained and sedentary animals. These data suggest that chronic aerobic exercise training can improve the Starling response in the presence of AT1 receptor blockade without altering absolute cardiac size.
引用
收藏
页码:3149 / 3154
页数:6
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