Titlebook: Biology of Vascular Smooth Muscle: Vasoconstriction and Dilatation; Yuansheng Gao Book 20171st edition Springer Nature Singapore Pte Ltd.

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Rechenbeispiele in der Transfusionsmedizin,ting membrane potentials of VSM cells, although being mainly determined by the equilibrium potential of K., are markedly affected by a high concentration of intracellular Cl.. The changes in membrane potentials associated with vasoconstriction are often graded depolarization rather than in action po

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https://doi.org/10.1007/978-3-211-89851-2derived hyperpolarizing factor (EDHF), and endothelin-1 (ET-1). The former three are vasodilators, while ET-1 is a potent vasoconstrictor. NO and PGI. exert their effects primarily by activating, respectively, cGMP–cGMP-dependent protein kinase (PKG) and cAMP–cAMP-dependent pathways, which result in

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https://doi.org/10.1007/978-3-642-74143-2d, therefore, are controlled by various complex yet coordinated mechanisms, in particular considering the marked difference in the concentrations across the cell membrane and across the membrane of the intracellular Ca. sarcoplasmic reticulum (SR). The major mechanisms for lowering the cytosolic Ca.

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https://doi.org/10.1007/978-3-642-74143-2mooth muscle cells, this interaction is predominantly regulated by the phosphorylation of the regulatory light chain (RLC) of myosin. The RLC is phosphorylated by myosin light chain kinase (MLCK) and dephosphorylated by myosin light chain phosphatase (MLCP). Therefore, the contractility of SMCs is d