The major findings of this work are as follows: (1) SHRcp display nondipper hypertension, differing from SHR, and are therefore a suitable animal model for studying the mechanism underlying abnormal circadian BP rhythm in MetS; and (2) it is likely that this disrupted circadian BP rhythm in SHRcp was at least in part attributed to angiotensin II–mediated autonomic dysfunction and enhanced aldosterone levels. This evidence concerns the gene AGT and metabolic syndrome.