BACKGROUND: Hypertension leads to cardiac hypertrophy as an adaptive response to 
increased workload. While initial development of hypertrophy is compensatory 
when contractile function is maintained, persistent stress on heart leads to 
deteriorated cardiac function and onset of heart failure. Mitochondrial 
dysfunction develops in the failing heart; however, whether it presents in 
compensatory cardiac hypertrophy is controversial.
METHODS: Spontaneously hypertensive rats (SHRs) and age-matched normotensive 
Wistar Kyoto rats were used in the study. Mitochondrial function and 
remodeling-related mechanisms in the left ventricles were measured by enzyme 
activity tests, Western blots, and reverse transcriptase polymerase chain 
reaction.
RESULTS: Compensatory cardiac hypertrophy in SHR was indicated by higher 
heart/weigh ratio, left ventricular systolic pressure and ±dp/dt(max) (P<.001, 
P<.05, and P<.01, respectively). Enzyme activities of mitochondrial complex I 
and II were significantly reduced (P<.05 and P<.01) in SHR in concert with 
decreased expression of complex subunits (P<.01 for NDUFS3, P=.068 for SDHB, and 
P<.05 for ATP5A1). Mitochondrial fission protein Drp1 was decreased (P<.05), 
while fusion protein OPA1 was increased (P<.01). Parkin and SirT1/AMPK-PGC-1α 
signaling, responsible for mitochondrial elimination and biogenesis 
respectively, were decreased in SHR (P<.01 for Parkin, P<.001 for SirT1 and 
p-AMPK).
CONCLUSION: Our results implicated that mitochondrial function and remodeling, 
indicated by mitochondrial enzyme activities and remodeling-related molecules, 
were compromised in compensatory hypertrophied myocardium of the SHR 
hypertensive model.
SUMMARY: Mitochondrial function in compensatory hypertrophied myocardium is 
controversial. Our present study found mitochondrial dysfunction in the left 
ventricle of spontaneously hypertensive rats, which was possibly a result of 
compromised mitochondrial remodeling including mitochondrial dynamics, 
elimination, and biogenesis.