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Valproate has a broad spectrum of anticonvulsant activity, although it is primarily used as a first-line treatment for tonic–clonic seizures, absence seizures and myoclonic seizures and as a second-line treatment for partial seizures and infantile spasms.
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Valproic acid, and its derivatives such as sodium valproate and divalproex sodium, causes cognitive deficit in the child, with an increased dose causing decreased intelligence quotient and use is associated with adverse neurodevelopmental outcomes (cognitive and behavioral) in children.
For example, a typical ER fluid can go from the consistency of a liquid to that of a gel, and back, with response times on the order of milliseconds. [1] The effect is sometimes called the Winslow effect after its discoverer, the American inventor Willis Winslow, who obtained a US patent on the effect in 1947 [ 2 ] and wrote an article ...
Compared with certain other L-type calcium channel blockers (for example those of the phenylalkylamine class such as verapamil) that have significant action at the heart, the dihydropyridine calcium channel blockers lower blood pressure mainly by relaxing the smooth muscle of the blood vessel walls. [3]
An example is Bay K8644, which is an analogue of nifedipine that specifically and directly activates L-type voltage-dependent calcium channels. [ 1 ] In contrast to Bay K8644, which is not for clinical use, ambroxol is a frequently used mucolytic drug that triggers lysosomal secretion by mobilizing calcium from acidic calcium stores. [ 2 ]
The basis for this broader spectrum of activity of lamotrigine is unknown but could relate to actions of the drug on voltage-gated calcium channels. Lamotrigine blocks T-type calcium channels weakly, if at all. However, it does inhibit native and recombinant high voltage-gated calcium channels (N- and P/Q/R-types) at therapeutic concentrations.
Thapsigargin raises cytosolic (intracellular) calcium concentration by blocking the ability of the cell to pump calcium into the sarcoplasmic and endoplasmic reticula. Store-depletion can secondarily activate plasma membrane calcium channels , allowing an influx of calcium into the cytosol.