To reveal the role of clock genes in generating the circadian rhythm of baroreflexes, we continuously measured mean arterial pressure and baroreflex sensitivity in free‐moving normal wild‐type mice, and in Cry‐deficient mice which lack a circadian rhythm, in constant darkness for 24 h. In wild‐type mice the mean arterial pressure was higher at night than during the day, and was accompanied by a significantly enhanced baroreflex sensitivity of −13.6 ± 0.8 at night compared with −9.7 ± 0.7 beats min⁻¹ mmHg⁻¹ during the day (P < 0.001). On the other hand, diurnal changes in arterial pressure disappeared in Cry‐deficient mice with remarkably enhanced baroreflex sensitivity compared with wild‐type mice (P < 0.001): −21.9 ± 1.6 at night and −23.1 ± 2.1 beats min⁻¹ mmHg⁻¹ during the day. Moreover, the mean arterial pressure response to 10 μg kg⁻¹ of phenylephrine, an α₁‐adrenoceptor agonist, was severely suppressed in Cry‐deficient mice regardless of time, while that for the wild‐type mice was 10.1 ± 1.9 mmHg in the night, significantly lower than 22.0 ± 3.5 mmHg in the day (P < 0.01). These results suggest that CRY genes are involved in generating the circadian rhythm of baroreflex sensitivity, partially by regulating α₁‐adrenoceptor‐mediated vasoconstriction in peripheral vessels.