In this article, we review briefly the available theories and data on [Ca2+]i-waves and [Ca2+]i-oscillations in mammalian cardiac and vascular smooth muscles. In addition to our review, we also report: (i) the existence and characterization of rapid agonist-induced [Ca2+]i-waves in cultured vascular smooth muscle cells (A7r5 cells); and (ii a new method for studying rapid [Ca2+]i-waves in mammalian cardiac ventricular cells. In mammalian cardiac muscle several types of Ca(2+)-release from sarcoplasmic reticulum (SR) are known to occur and might be involved in Ca(2+)-waves and Ca(2+)-oscillations: (a) Ca(2+)-induced release of Ca2+, of the type thought to be important in normal excitation-contraction coupling; (b) spontaneous, cyclic release of Ca2+ related to a Ca(2+)-overload of the SR; and (c) Ins(1,4,5)P3-induced Ca(2+)-release. The available data support the idea that [Ca2+]i-waves in heart propagate by a mechanism somewhat different than that involved in normal excitation-contraction coupling (a, above), perhaps involving spontaneous release of Ca2+ from an overloaded SR (b, above). In mammalian vascular smooth muscle, our data support the idea that agonist-receptor interaction (vasopressin, in this case) initiates [Ca2+]i-waves that then propagate via some form of Ca(2+)-induced release of Ca2+, perhaps in a manner similar to that proposed by Berridge and Irvine [1].