OBJECTIVES: To follow the development of left ventricular structure and function in vivo in two different models of pressure-overload hypertrophy. DESIGN: From age 6 weeks, left ventricular structure and function changes in spontaneously hypertensive (SHR) and renal hypertensive (RHR) rats were followed in vivo by magnetic resonance imaging over 7 months. Wistar-Kyoto rats served as controls. METHODS: Systolic blood pressure (SBP) was measured once a week by the tail-cuff method. Transverse left ventricular sections were obtained at end-diastole and end-systole by electrocardiogram-gated magnetic resonance imaging, allowing the determination of left ventricular mass, wall thickness and volume. Angiotensin II (Ang II) plasma levels were determined at 2 and 4 weeks into the study. At the end of the study functional parameters were obtained by left ventricular catheterization. RESULTS: After 4 weeks both SHR and RHR showed a similar degree of hypertension. At 4 weeks Ang II levels were significantly elevated in RHR and suppressed in SHR relative to controls. The extent of left ventricular hypertrophy was essentially the same in SHR and RHR, but the diastolic left ventricular wall thickness: volume ratio was substantially increased in RHR only. During the first 11 weeks of the study, a small end-systolic volume and an increased end-systolic wall thickness allowed the systolic wall stress in RHR to be maintained near control values. Thereafter a discrete deterioration of left ventricular function was observed, as demonstrated by the steady increase in end-systolic volume. In contrast, SHR did not show an increase in end-systolic wall thickness at any time, resulting in an elevated systolic wall stress. However, left ventricular function was stable during the observed period. CONCLUSION: Despite similar SBP and left ventricular mass, left ventricular remodelling and function were different in RHR and SHR. SHR appeared to be stable during the 30-week observation period, whereas RHR exhibited a progressive functional impairment after week 11. The distinct involvement of the renin-angiotensin system in the pathogenesis of hypertension in these models may account for these differences.
OBJECTIVES: To follow the development of left ventricular structure and function in vivo in two different models of pressure-overload hypertrophy. DESIGN: From age 6 weeks, left ventricular structure and function changes in spontaneously hypertensive (SHR) and renal hypertensive (RHR) rats were followed in vivo by magnetic resonance imaging over 7 months. Wistar-Kyoto rats served as controls. METHODS: Systolic blood pressure (SBP) was measured once a week by the tail-cuff method. Transverse left ventricular sections were obtained at end-diastole and end-systole by electrocardiogram-gated magnetic resonance imaging, allowing the determination of left ventricular mass, wall thickness and volume. Angiotensin II (Ang II) plasma levels were determined at 2 and 4 weeks into the study. At the end of the study functional parameters were obtained by left ventricular catheterization. RESULTS: After 4 weeks both SHR and RHR showed a similar degree of hypertension. At 4 weeks Ang II levels were significantly elevated in RHR and suppressed in SHR relative to controls. The extent of left ventricular hypertrophy was essentially the same in SHR and RHR, but the diastolic left ventricular wall thickness: volume ratio was substantially increased in RHR only. During the first 11 weeks of the study, a small end-systolic volume and an increased end-systolic wall thickness allowed the systolic wall stress in RHR to be maintained near control values. Thereafter a discrete deterioration of left ventricular function was observed, as demonstrated by the steady increase in end-systolic volume. In contrast, SHR did not show an increase in end-systolic wall thickness at any time, resulting in an elevated systolic wall stress. However, left ventricular function was stable during the observed period. CONCLUSION: Despite similar SBP and left ventricular mass, left ventricular remodelling and function were different in RHR and SHR. SHR appeared to be stable during the 30-week observation period, whereas RHR exhibited a progressive functional impairment after week 11. The distinct involvement of the renin-angiotensin system in the pathogenesis of hypertension in these models may account for these differences.