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Calcium Dependent Regulation of Vascular Smooth Muscle Contraction

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Cellular and Molecular Mechanisms in Hypertension

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 308))

Abstract

It is well established that an increase in cytosolic free calcium (Ca2+) initiates contraction of smooth muscle, but precisely how this transduction occurs is a subject of considerable debate. Two significant advances in our understanding of the biochemical regulation of smooth muscle contraction, made in the mid 1970’s, served as the basis for many subsequent investigations. In 1974, Bremel demonstrated that the primary Ca2+ dependence of vertebrate smooth muscle contraction is associated with the thick filament, rather than the thin filament which is the case for striated muscle (1). Later, Sobieszek (2) and Aksoy et al. (3) independently demonstrated that the Ca2+ sensitivity of actomyosin ATPase activity was associated with phosphorylation of the 20,000 Mr myosin light chain (MLC). Phosphorylation of the MLC resulted from the activation of a Ca2+ and calmodulin dependent enzyme, the MLC kinase (4). The demonstration of a direct correlation between MLC phosphorylation and both Ca2+ dependent actin-activated myosin ATPase activity (2,3,5) and force development in either skinned (6,7) or intact (8,9) muscle fibers has resulted in an almost universal acceptance of this system as the primary regulator of smooth muscle contraction.

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© 1991 Plenum Press, New York

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Moreland, R.S., Cilea, J., Moreland, S. (1991). Calcium Dependent Regulation of Vascular Smooth Muscle Contraction. In: Cox, R.H. (eds) Cellular and Molecular Mechanisms in Hypertension. Advances in Experimental Medicine and Biology, vol 308. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-6015-5_7

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  • DOI: https://doi.org/10.1007/978-1-4684-6015-5_7

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-6017-9

  • Online ISBN: 978-1-4684-6015-5

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