Essential hypertension (EH) is an escalating problem for developed and developing countries. It is currently seen as a ‘complex’ genetic trait caused by multiple susceptibility genes which are modulated by gene-environment and gene-gene interactions. Over the past 10 years, mitochondrial defects have been implicated in a wide variety of degenerative diseases, aging, and cancer. Recently several studies showed that human essential hypertension has excess maternal transmission which suggests a possible mitochondrial involvement. However, the exact pathophysiology of mitochondrial DNA mutation (mtDNA) in essential hypertension still remains
perplexing. With the application of a variety of imaging approaches and successive mouse model of mitochondrial diseases we convince that these problems will be resolved in the near future.