Vascular smooth muscle cells are important sensors and regulators of circumferential wall tension which triggers their contraction in response to an increase in transmural pressure (e.g. hypertension). Interestingly, genetic ablation of Junb – encoding the corresponding subunit of the transcription factor activator protein 1 (AP-1) – in mice abolishes the development of hypertension upon DOCA-salt treatment but does not prevent remodelling of the vessel wall. Subsequent analysis of isolated perfused Junb-deficient arteries revealed a diminished contractile capacity in response to increasing intraluminal pressure or stimulation with norepinephrine. As contraction of smooth muscle cells is dependent on the activity of the actin-myosin complex and the formation of actin stress fibers, we consequently analysed these responses in cultured murine smooth muscle cells. In line with the aforementioned observations, stretch-induced stress fiber formation and the expression of myosin light chain 2 (MLC2) were impaired in Junb-deficient vascular smooth muscle cells. Taken together, our data revealed an essential role of the AP-1 transcription factor subunit Junb in maintaining arterial contractility hence tone by controlling transcription of MLC2.