Smooth muscles as a group are defined by the absence of a sarcomeric organisation of their contractile proteins. Great strides have been made in the last 25 years in understanding the functions and physiologies of these relatively small muscle cells. The development of enzyme techniques enabling dispersion of smooth muscle tissues into constituent myocytes has enabled their complement of plasmalemmal ion channels to be studied by single-cell tight-seal voltage-clamp technique. This, combined with high resolution light microscopy of living cells using fluorescent indicators and tags, have enabled us to understand much more about the process of excitation-contraction coupling in smooth muscles. Almost all smooth muscles seem to possess voltage-dependent calcium channels (VDCCs) and calcium-activated potassium (BKCa) channels. However despite this, their electrical activity may be very different. Some readily and often spontaneously discharge action potentials which propagate from cell to cell, travelling limited distances through the muscle tissue: others seldom discharge action potentials but nevertheless they are electrically coupled and calcium entry into the cell through VDCCs is generally very important in controlling tension generation. Because smooth muscles lack sarcomeres, the mechanisms for release of calcium from, and restoration into, the calcium stores (or its extrusion from the cell) cannot resemble striated muscles. SMCs have instead developed a system of preferred sarcoplasmic reticulum (SR) release sites from which calcium is initially released upon the arrival of a stimulus. This may take the form of an action potential, or the activation of a (generally G-protein coupled) receptor, or commonly, a combination of these two mechanisms. The interactions of these two systems provides a basis for our understanding of excitation-contraction coupling in all smooth muscles. There is great interest in the relationship of caveolae to receptors, ion channels and calcium release sites. In addition, many smooth muscles have a process whereby calcium is released in packets from the SR when these become overloaded; the transient high localised calcium concentration created in a subplasmalemmal location acts to cause bursts of BKCa channel openings giving rise to spontaneous transient outward currents (STOCs) which hyperpolarize the membrane but negligibly increase cytoplasmic calcium concentration. In some smooth muscles, similar bursts of openings of calcium-activated chloride channels are believed to be the basis of spontaneous pacemaker potentials. These negative and positive feedback processes contribute substantially to the properties of various smooth muscles. However, smooth muscles as a group are extremely diverse in their complement of receptor types, their innervation, contractile properties and physiological function. The future holds the promise that we will begin to understand how this diversity arises by tracking the expression of genes which control variations on these common themes, so providing an explanation of the unique physiological properties of each smooth muscle type.