Neurotransmitters as well as other mediators bind to receptors initiating signals directed to ion channels and second messenger generating mechanisms that initiate smooth muscle contraction. Current evidences indicate that an increase in intracellular calcium ([Ca2+]i) is the usual intracellular signal for initiating contraction. The source of Ca2+ available to initiate contraction in smooth muscle may be extracellular as well as intracellular depending upon the source of smooth muscle, cellular environment and the nature of the stimulus. Thus, the increase of [Ca2+]i for contraction may be achieved by the influx of Ca2+ via Ca2+ channels that open upon the plasma membrane (PM) potential changes (electro-mechanical coupling, EMC) or ligand-gated, membrane potential-independent mechanisms (pharmaco-mechanical coupling, PMC), and, by the release of intracellularly sequestered Ca2+ from internal Ca2+ stores, typically the endoplasmic reticulum (ER) or sarcoplasmic reticulum (SR). To achieve and maintain a state of relaxation (usually requiring a [Ca2+]i < l0-7M), requires balancing of an inward leak of Ca2+ down the electrochemical gradient since this leak is present even when voltage- or receptor-operated channels are closed. Mechanisms for extrusion or sequestration of the cytosolic Ca2+ need to be activated to reduce the [Ca2+]i. Both PM and SR participate in lowering [Ca2+]i under physiological conditions. However, it has been and remains technically difficult to clearly dissociate events initiated at the level of PM and those at the level of SR during excitation-contraction coupling in smooth muscle (see for review Daniel et al., 1983).
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