Electro- and Pharmacomechanical Coupling in Vascular Smooth Muscle

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The resting membrane potential of vascular smooth muscle cells depends largely on the building up of ion gradients and also to some extent on the function of an electrogenic ion pump. However, the role of this membrane potential in determining the mechanical activity of the tissue is rather limited and substances such as noradrenaline and histamine can induce contraction without or with only a limited depolarization of the membrane. This pharmacomechanical coupling is therefore considered the predominant regulatory system in vascular smooth muscle contraction. The absence of action potentials in most of these tissues seems to depend on the rectifying properties of the cell membrane for outward current. The contractile proteins are activated by an increase of the cytoplasmic calcium (Ca), which is supplied from the external membrane and/or from the intracellular Ca store. It is an attractive hypothesis to assume that the outer membrane presents voltage dependent Ca channels which can be activated by depolarization and receptor operated channels which are activated by alpha agonists. Such agonists can also release at the same time Ca from the intracellular stores. The relaxation of the tissue depends on the reuptake of Ca by the intracellular store and on a Ca extrusion across the cell membrane. Some evidence is brought forward that in vascular smooth muscle an ATP-dependent Ca pump is more likely then a Na-Ca exchange mechanism.