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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 basal 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 1 μM ouabain, or of the Na+/Ca2+ exchanger (NCX) with 1 μM KB-R 7943, did not abolish the calcium oscillations, thus showing that these two pumps are only modulatory elements, while on the other hand, voltage-gated calcium channels have been found to be important in the vasomotion mechanism.