Abstract
Maintained calcium influx into vascular smooth muscle through voltage-dependent calcium channels plays a key role in the control of the intracellular free calcium ion concentration ([Ca2+]i), and hence the contractile state of arterial smooth muscle cells (e.g. 12). Agents that depolarize (e.g. elevated extracellular potassium, pressurization, many vasoconstrictors) cause arteries to constrict. This tone is often reduced or abolished by removing extracellular calcium, organic calcium entry blockers or membrane hyperpolarization (11, 12, 13). Although other processes are clearly important in regulating vascular tone (for example regulation of intracellular calcium release, calcium extrusion, or the calcium-force relationship), these results strongly suggest that calcium entry through dihydropyridine-sensitive calcium channels is necessary for maintained tone development in many cases, and that the membrane potential dependence of arterial tone arises from the voltage-dependence of the calcium channel (12).
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Quayle, J.M., Nelson, M.T. (1993). Calcium Channels in Arterial Smooth Muscle Cells. In: Weir, E.K., Hume, J.R., Reeves, J.T. (eds) Ion Flux in Pulmonary Vascular Control. NATO ASI Series, vol 251. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2397-0_3
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