Intracellular Ca(2+) signaling is important to perfusion pressure related arterial reactivity and to vascular disorders including hypertension, angina and ischemic stroke. We have recently shown that advancing-age leads to calcium signaling adaptations in mesenteric arterial myocytes from C57 BL/6 mice [Corsso, C.D., Ostrovskaya, O., McAllister, C.E., Murray, K., Hatton, W.J., Gurney, A.M., Spencer, N.J., Wilson, S.M., 2006. Effects of aging on Ca(2+) signaling in murine mesenteric arterial smooth muscle cells. Mech. Ageing Dev. 127, 315-323)] which may contribute to decrements in perfusion pressure related arterial contractility others have shown occur. Even still, the mechanisms underlying the changes in Ca(2+) signaling and arterial reactivity are unresolved. Ca(2+) transport and storage capabilities are thought to contribute to age-related Ca(2+) signaling dysfunctions in other cell types. The present studies were therefore designed to test the hypothesis that cytosolic and compartmental Ca(2+) homeostasis in mesenteric arterial myocytes changes with advanced age. The hypothesis was tested by performing digitalized fluorescence microscopy on mesenteric arterial myocytes isolated from 5- to 6-month and 29- to 30-month-old C57Bl/6 mice. The data provide evidence that with advanced age capacitative Ca(2+) entry and sarcoplasmic reticulum Ca(2+) storage are increased although sarcoplasmic reticulum Ca(2+) uptake and plasma membrane Ca(2+) extrusion are unaltered. Overall, the studies begin to resolve the mechanisms associated with age-related alterations in mesenteric arterial smooth muscle Ca(2+) signaling and their physiological consequences.