Mitochondrial abnormalities in hypertrophied myocardium of stroke-prone spontaneously hypertensive rats.

Abstract

1. To clarify the pathogenesis of cardiac disorders in SHRSP which showed severe cardiac hypertrophy and myocardial degeneration in the hypertensive stage, restriction fragment length polymorphisms (RFLP) of mitochondrial DNA (mtDNA), and morphological and functional changes of mitochondria were examined. 2. Morphologically, the mitochondrial size showed a wider range of distribution in SHRSP both at prehypertensive and hypertensive stage compared to those in age-matched WKY. 3. Isocitrate dehydrogenase (ICDH) activity, but not superoxide dismutase (SOD) activity, was higher in the young SHRSP, whereas both enzyme activities were lower in the mature SHRSP than in the age-matched WKY. 4. RFLP analysis by electrophoresis revealed that the loss of two restriction sites for Rsa I in the myocardial mtDNA from the SHRSP, but not in that from the WKY. 5. These findings suggest that the structural changes of mtDNA could be related, at least partly, to morphological and functional changes of mitochondria in the SHRSP myocardium.