Titlebook: Signal Transduction and the Gasotransmitters; NO, CO, and H2S in B Rui Wang Book 2004 Springer Science+Business Media New York 2004 ATP.Cal

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Nitric Oxide and Voltage-Gated Ca2+ Channelsm intracellular stores. There is a large body of experimental evidence indicating that all mechanisms controlling the intracellular Ca. concentrations are regulated by NO. In excitable cells, activation of the voltage-gated Ca. channels is certainly the most effective means of generating Ca. influx

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Synthesis and Metabolism of Carbon Monoxideme molecule in vital cellular processes. CO, though chemically inert, acts as a heme iron ligand. Living organisms acquire CO by inhalation, by endogenous enzymatic heme degradation catalyzed by heme oxygenases (HOs), or as a byproduct of lipid and xenobiotic metabolism. The HO enzymes exist in both

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Interaction of Carbon Monoxide With K+ Channels in Vascular Smooth Muscle Cellsnd lowers peripheral resistance, thus influencing the homeostatic control of blood pressure. Stimulation of various types of K. channels in vascular smooth muscle cells (VSMCs) is one of the mechanisms for the CO-induced vasorelaxation. These K. channels include voltagedependent Kv, adenosine tripho

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The Molecular Mechanisms Underlying the Effects of Carbon Monoxide on Calcium-Activated K+ ChannelsVSMCs), the opening of BK. channels provides a negative feedback in response to membrane depolarization and increased intracellular calcium. Consequent membrane hyperpolarization and closure of voltage-dependent calcium channels leads to relaxation of VSMCs. In this context, a better understanding o

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Carbon Monoxide and Signal Transduction Pathways CO is a diatomic gas that is generated predominantly from heme degradation by the enzyme heme oxygenase. Traditionally considered a biological “waste product” of heme metabolism and, at high doses, lethal, CO clearly has diverse functions including the modulation of neural signals, inflammation, ce

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