smoothmuscle bmal1 participates in blood pressure circadian rhythm regulation as the central pacemaker the suprachiasmatic nucleus scn has long been considered the primary regulator of blood pressure circadian rhythm however this dogma has been challenged by the discovery that each of the clock genes present in the scn is also expressed and functions in peripheral tissues the involvement and contribution of these peripheral clock genes in the circadian rhythm of blood pressure remains uncertain here we demonstrate that selective deletion of the circadian clock transcriptional activator aryl hydrocarbon receptor nuclear translocatorlike bmal1 from smooth muscle but not from cardiomyocytes compromised blood pressure circadian rhythm and decreased blood pressure without affecting scncontrolled locomotor activity in murine models in mesenteric arteries bmal1 bound to the promoter of and activated the transcription of rhokinase 2 rock2 and bmal1 deletion abolished the timeofday variations in response to agonistinduced vasoconstriction myosin phosphorylation and rock2 activation together these data indicate that peripheral inputs contribute to the daily control of vasoconstriction and blood pressure and suggest that clock gene expression outside of the scn should be further evaluated to elucidate pathogenic mechanisms of diseases involving blood pressure circadian rhythm disruption