Artery narrowing in hypertension can only result from structural remodelling of the artery, or increased smooth muscle contraction. The latter may occur with, or without, increases in [Ca2+]i. Here, we sought to measure, in living hypertensive mice, possible changes in artery dimensions and/or [Ca2+]i, and to determine some of the mechanisms involved. Ca2+/calmodulin biosensor (Förster resonance energy transfer-based) mice were made hypertensive by s.c. infusion of angiotensin II (Ang II, 400 ng kg−1 min−1, 2–3 weeks). Intravital fluorescence microscopy was used to determine [Ca2+]i and outer diameter of surgically exposed, intact femoral artery (FA) of anaesthetized mice. Active contractile FA ‘tone’ was calculated from the basal-state diameter and the passive (i.e. Ca2+-free) diameter (PD). Compared to saline control, FAs of Ang II-infused mice had (1) ∼21% higher active tone and (2) ∼78 nm higher smooth muscle [Ca2+]i, but (3) the same PDs. The local Ang II receptor (AT1R) blocker losartan had negligible effect on tone or [Ca2+]i in control FAs, but reduced the basal tone by ∼9% in Ang II FAs. Both i.v. hexamethonium and locally applied prazosin abolished the difference in FA tone and [Ca2+]i, suggesting a dominant role of sympathetic nerve activity (SNA). Changes in diameter and [Ca2+]i in response to locally applied phenylephrine, Ang II, arginine vasopressin, elevated [K+]o and acetylcholine were not altered. In summary, FAs of living Ang II hypertensive mice have higher [Ca2+]i, and are more constricted, due, primarily, to elevated SNA and some increased arterial AT1R activation. Evidence of altered artery reactivity or remodeling was not found.