Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as 
elementary calcium release events (calcium sparks) associated with the opening 
of L-type Ca(2+) channels. In heart cells, a tight coupling between the gating 
of single L-type Ca(2+) channels and ryanodine receptors (RYRs) underlies 
calcium release. Here we demonstrate that L-type Ca(2+) channels activate RYRs 
to produce CICR in smooth muscle cells in the form of Ca(2+) sparks and 
propagated Ca(2+) waves. However, unlike CICR in cardiac muscle, RYR channel 
opening is not tightly linked to the gating of L-type Ca(2+) channels. L-type 
Ca(2+) channels can open without triggering Ca(2+) sparks and triggered Ca(2+) 
sparks are often observed after channel closure. CICR is a function of the net 
flux of Ca(2+) ions into the cytosol, rather than the single channel amplitude 
of L-type Ca(2+) channels. Moreover, unlike CICR in striated muscle, calcium 
release is completely eliminated by cytosolic calcium buffering. Thus, L-type 
Ca(2+) channels are loosely coupled to RYR through an increase in global 
[Ca(2+)] due to an increase in the effective distance between L-type Ca(2+) 
channels and RYR, resulting in an uncoupling of the obligate relationship that 
exists in striated muscle between the action potential and calcium release.