Calcium channels concentration reductions

The inhibitory effect of a2 agonists on noradrenaline release involves a hyperpolarization of the presynaptic membranes by opening potassium ion channels. The reduction in the release of noradrenaline following the administration of an a2 agonist is ultimately due to a reduction in the concentration of free cytosolic calcium, which is an essential component of the mechanism whereby the synaptic vesicles containing noradrenaline fuse to the s)maptic membrane before their release. 

It is now obvious that the contraction of smooth muscle is controlled by the concentration of calcium in the cytoplasm. A basic principle of calcium-channel blocker action is that they disturb diffusion of calcium into muscle cells of the heart and vessels. Reduction of calcium ions entering the cells of the myocardium leads to a reduced use of the energy of phosphate bonds for mechanical heart work. As a result, strength of cardiac contractions and heart work are reduced, which in turn leads to a reduction in the heart s need of oxygen. 

L-Type calcium channel blockers, verapamil (5 mg/kg i.p.) and nifedipine (5 mg/kg i.p.) enhanced L-2-propionic acid (750 mg/kg per os)-induced rat granule cell necrosis, assessed by measuring the degree of L-2-propionic acid-induced reductions aspartate concentrations, increases in cerebellar... 

In cell culture preparations, diphenylhydantoin, carbamazepine and valproate have been shown to reduce membrane excitability at therapeutically relevant concentrations. This membrane-stabilizing effect is probably due to a block in the sodium channels. High concentrations of diazepam also have similar effects, and the membrane-stabilizing action correlates with the action of these anticonvulsants in inhibiting maximal electroshock seizures. Intracellular studies have shown that, in synaptosomes, most anticonvulsants inhibit calcium-dependent calmodulin protein kinase, an effect which would contribute to a reduction in neurotransmitter release. This action of anticonvulsants would appear to correlate with the potency of the drugs in inhibiting electroshock seizures. The result of all these disparate actions of anticonvulsants would be to diminish synaptic efficacy and thereby reduce seizure spread from an epileptic focus. 

The primary reaction of alkali with reservoir water is to reduce the activity of multivalent cations such as calcium and magnesium in oilfield brines. Upon contact of the alkali with these ions, precipitates of calcium and magnesium hydroxide, carbonate, or silicate may form, depending on pH, ion concentrations, temperature, and so on. If properly located, these precipitates can cause diversion of flow within the reservoir, leading to better contact of the injected fluid with the less-permeable and/or less-flooded flow channels. This then may contribute to improved recovery. Also, this reduction of reservoir brine cation activity will lead to more surfactant activity, resulting in lower IFT values (Mayer et al., 1983). 

It is established that Ca + and K+ are involved in maintenance and termination of the plateau phase of the cardiac action potential. Furthermore, intracellular calcium concentration controls membrane K+ permeability via the various conductance components for K+ (gK], gK2, glx) (69) It is also established that action potential duration and myocardial tension development are integrally related (13). In view of previous observations and explanations for the excitation-contraction coupling process and the effects of calcium inhibitory compounds upon the cardiac action potential of ventricular muscle and Purkinje fibers, one possible explanation for the effects observed in ventricular muscle preparations is that low concentrations of calcium inhibitory compounds reduce the amount of intracellular free calcium in the vicinity of the K+ channel, thereby changing the channel s configuration resulting in a reduction in gK+ and delayed repolarization of the ventricular muscle action potential. 

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