Smooth muscle cell calcium dynamics and diameter were measured in intact pressurized rat mesenteric artery segments during vasoconstriction and vasomotion. Arteries showed a certain norepinephrine (NE) threshold (0.3-0.4 μM) for the onset of vasomotion, during a cumulative NE concentration-response curve. This was due to a necessary [Ca²⁺]_i threshold (increase over basel level of 22.2 ± 2.6%) to elicit oscillations. The calcium oscillations obtained were synchronous over the entire vessel length and phase-shifted (in advance by 1.7 ± 0.3 seconds) with respect to the diameter oscillations. A similar result was obtained using a KCl depolarization to contract the arteries, even though the [Ca²⁺]_i threshold was much smaller in this case (increase over basal level of 9.9 ± 4.3%), as compared with the NE-elicited vasomotion. Blockade of the NA⁺/K⁺-ATPase with l μM ouabain, or of the Na⁺/Ca⁺exchanger (NCX) with l μM KB-R 7943, did not abolish the calcium oscillation, while on the other hand, voltage-gated calcium channels have been found to be important in the vasomotion mechanism.