Abstract
Hyperhomocysteinemia (HHcy) is a risk factor for hypertension which is associated with aortic and cardiovascular pathologies. Although the exact underlying mechanisms are still not clear, emerging evidence implicates a role of epigenetic regulation. We hypothesize that 5 Aza 2 deoxycytidine (5 Aza dC), DNMT inhibitor, lowers blood pressure by regulating methylation levels in HHCy. Wild type (WT) and CBS +/− (HHcy) mice were administered with 5 Aza dC (0.5mg/kg body weight, DNA methyl transferase (DNMT) inhibitor), for four weeks. Blood pressure measured using tail cuff and radio telemetry methods showed a significant decrease in CBS +/− mice following treatment. mRNA expression levels of DNMTs were found to be lower in CBS+/− treatment group when compared to controls. Aortic vessel reactivity was increased in myobath studies following treatment with 5 Aza dC. Ultrasound revealed an increase in abdominal and ascending aorta diameter in treated CBS +/− mice. We conclude that inhibition of DNMT, 5 Aza dC, lowers blood pressure by regulating methylation levels in HHcy and has therapeutic potential in hypertension.
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