Excessive activation of the AT(1A) receptor (AT(1A)R) by angiotensin II (Ang II) is implicated in the age-related development of hypertension, diabetes, and kidney disease. AT(1A)R-deficient mice live longer and have lower levels of oxidative stress than wild-type mice (Benigni et al., 2009), suggesting a role for AT(1A)R signaling in the aging process.