ABSTRACT
As in all other types of muscles, calcium is the critical signal for initiating and maintaining contractions of smooth muscle (SM) cells. However, in comparison to skeletal and cardiac muscles, SM appears to be especially enriched with a multitude of ion channels that function in concert to regulate Ca2+ inŸux and thus the intracellular free calcium concentration ([Ca2+]i). Under physiological conditions, changes in SM tension (either contraction or reduction of existing tone) are usually induced by, or at least associated with, changes in the membrane potential. Thus, SM excitation in the form of action potentials in those types of SM capable of generating them or in the form of more slowly developing potential changes in less excitable or nonexcitable SM (e.g., slow waves) causes Ca2+ entry via voltage-gated Ca2+ channels (VGCCs). This, in turn, can trigger Ca2+-induced Ca2+ release (CICR), bringing an additional source of Ca2+ into action. Similarly, membrane hyperpolarization causes SM relaxation by inhibiting action potential discharge and reducing activity of VGCCs.
