The mechanism for blood pressure elevation in newly developed obesity mouse and the application for the prevention and treatment of hypertension

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We generated conventional knockout mice (KO) of sequestosome1/A170, the molecule related to oxidative stress. KO exhibited the phenotype of obesity and impaired glucose tolerance due to hyperphagia and leptin resistance. We evaluated hemodynamics by telemetry system under no restrictions. During resting time, blood pressure (BP) and pulse rate was higher in KO compared to wild type (WT) though it did not differ during active time, indicating that KO shows the BP pattern of non-dipper type of hypertension. The urine amount of excreted catecholamine was significantly higher in KO than WT, suggesting that increase of the sympathetic nerve activity contributes to the BP elevation in KO.