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Arterial levels for drugs are generally higher than venous levels because of extraction while passing through tissues. ... Ionized calcium (Ca) 1.03, [20] 1.10 [5] 1. ...
Extracellular calcium levels are approximated to be 12000-fold greater than intracellular levels. During calcium-dependent processes, the intracellular level of calcium rises by up to 100-fold. It is vitally important to regulate this calcium gradient, not least because high levels of calcium are toxic to the cell, and can induce apoptosis. Ca ...
A calcium channel is an ion channel which shows selective permeability to calcium ions. It is sometimes synonymous with voltage-gated calcium channel, [1] which are a type of calcium channel regulated by changes in membrane potential. Some calcium channels are regulated by the binding of a ligand.
Though calcium is the most plentiful electrolyte in the body, a large percentage of it is used to form the bones. [14] It is mainly absorbed and excreted through the GI system. [14] The majority of calcium resides extracellularly, and it is crucial for the function of neurons, muscle cells, function of enzymes, and coagulation. [14]
Calcium-activated potassium channels are potassium channels gated by calcium, [1] or that are structurally or phylogenetically related to calcium gated channels. They were first discovered in 1958 by Gardos [who?] who saw that calcium levels inside of a cell could affect the permeability of potassium through that cell membrane. Then in 1970 ...
This gene encodes Ca v 3.2, a T-type member of the α 1 subunit family, a protein in the voltage-dependent calcium channel complex. Calcium channels mediate the influx of calcium ions into the cell upon membrane polarization and consist of a complex of α 1, α 2 δ, β, and γ subunits in a 1:1:1:1 ratio.
The calcium binds to the calcium release channels (RYRs) in the SR, opening them; this phenomenon is called "calcium-induced calcium release", or CICR. However the RYRs are opened, either through mechanical-gating or CICR, Ca 2+ is released from the SR and is able to bind to troponin C on the actin filaments.
In the arteries of the brain, high levels of calcium in mitochondria elevates activity of nuclear factor kappa B NF-κB and transcription of CACNA1c and functional Cav1.2 expression increases. [12] Cav1.2 also regulates levels of osteoprotegerin. [13] Ca V 1.2 is inhibited by the action of STIM1. [14]
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