Abstract
Vascular smooth muscle contraction is triggered by a rise in the intracellular free Ca2+ concentration, the amplitude of the contractile activity being dependent on the magnitude of the calcium signal. The change in the Ca2+ concentration can be due to an increased influx of Ca2+ from the extracellular space or to a release of Ca2+ from intracellular stores. The influx of Ca2+ occurs via two seperate pathways, i.e. through voltage dependent Ca2+ channels which are opened by depolarization of the cell membrane, and receptor-operated calcium channels which are opened by the interaction of agonists with their receptors. In contrast to striated musclss activation of smooth muscle involves the reversible phosphorylation of myosin by a specific kinase, the myosin light chain kinase which is activated by Ca2+ via the intracellular calcium receptor calmodulin. Although Ca2+ is the major determinant of the contractile activity, the response of the contractile apparatus to Ca2+ can be modulated over a wide range. Modulators are H+ -ions and inorganic phosphate. Wich may accumulate during hypoxia, and the cyclic nucleotide cAMP and cGMP which play an important role in vasodilation. The relation ship between Ca2+ and contraction may also be modulated by certain drugs (e.g. calcium antagonists).
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Pfitzer, G. 16 Calcium and vascular smooth muscle contraction. Pediatr Res 20, 1036 (1986). https://doi.org/10.1203/00006450-198610000-00070
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DOI: https://doi.org/10.1203/00006450-198610000-00070