The role of membrane potential-dependent and independent regulation of the intracellular free calcium concentration ([Ca2+]i) was assessed in the mesenteric small arteries of Wistar rats. [Ca2+]i was determined by Fura-2 fluorescence. Membrane potential measurements were made using intracellular microelectrodes. Depolarization with a high-potassium solution (K-PSS) elevated [Ca2+]i and induced contraction. Further addition of 10 µM noradrenaline (NA) did not elevate [Ca2+]i further but enhanced tone. Addition of calcium channel inhibitors (felodipine or D-600) inhibited the maintained rise in [Ca2+]i with K-PSS, but NA still elevated [Ca2+]i and force to about half the previous level. Further addition of either ryanodine or thapsigargin eliminated the rise in [Ca2+]i with NA, although 10–20% of the contraction remained. Simultaneous measurements of membrane potential, [Ca2+]i, and force during cumulative additions of NA or K-PSS in the absence of inhibitors showed similar relations between membrane potential and [Ca2+]i for each means of activation. The results indicate that membrane potential and [Ca2+]i are strongly correlated in mesenteric small arteries. A small part of the [Ca2+]i increase to NA can be attributed to release from intracellular stores. Membrane potential-independent calcium channels that are directly operated by adrenoceptors appear to play a minor role in the regulation of [Ca2+]i in these vessels.