Ca2+ regulate the contractility in VSMCs, alter the local circulation and would finally modify the sBP. To elucidate the contribution of Ca2+i in VSMCs of mesenteric artery and vasoconstriction of resestance artery to the sBP, we constructed a novel modality to simultaneously monitor the in vivo Ca2+i in VSMCs after loading fura-2, internal diameter(ID) and mean sBP of rats under urethan anesthesia. Even before the application of vasoactive agent, the Ca2+i showed a weak but definite OS(~2/min.), spontaneously synchronizing with the Ca2+i of the adjacent VSMCs. It accompanied a repetitive contraction of the artery but no change in the sBP at all. After i.v. application of noradrenalin(50μg/kg), the Ca2+i in all VSMCs increased at 5 sec., peaked at 15 sec., then declined and returned to the basal level at 1.5 min. In the declining phase, the Ca2+i demonstrated spiky OS in VSMCs(~15/min.) and it did not synchronize with that of adjacent VSMCs. The ID started to reduce with 2 sec delay to the Ca2+i, reached to the minimum at 30 sec.and returned to the basal value at 2 min.without any alternating pattern. The sBP revealed a complete mirror image to the ID, indicating that , not the Ca2+i in individual cells, but, constriction of the resistance artery was directly reflected to the sBP. Thus, the present method may provide a new insight for vascular physiology, as represented by the two different Ca2+i oscillation systems in VSMC. Details of the results will be displayed in video.