Calcium influx

Consistent with the abiUty of vinpocetine to act as an anticonvulsant is its abiUty to inhibit cellular reuptake of adenosine (15) which has been described as the brain s endogenous anticonvulsant because of its abiUty to inhibit calcium influx. Thus the property of vinpocetine to inhibit adenosine reuptake maybe responsible for the neuroprotective actions of the dmg. 

Another mechanism in initiating the contraction is agonist-induced contraction. It results from the hydrolysis of membrane phosphatidylinositol and the formation of inositol triphosphate (IP3)- IP3 in turn triggers the release of intracellular calcium from the sarcoplasmic reticulum and the influx of more extracellular calcium. The third mechanism in triggering the smooth muscle contraction is the increase of calcium influx through the receptor-operated channels. The increased cytosolic calcium enhances the binding to the protein, calmodulin [73298-54-1]. 

Calcium channel blockers reduce arterial blood pressure by decreasing calcium influx, resulting in a decrease in intracellular calcium (236,237). The arterial smooth muscle tone decreases, thereby decreasing total peripheral resistance. The increase in vascular resistance in hypertension is found to depend much on calcium influx. Calcium channel blockers reduce blood pressure at rest and during exercise. They decrease the transmembranous calcium influx or entry that lead to a net decrease of intracellular calcium and therefore the vascular tone falls, as does blood pressure. 

Diltiazem inhibits calcium influx via voltage-operated channels and therefore decreases intracellular calcium ion. This decreases smooth muscle tone. Diltiazem dilates both large and small arteries and also inhibits a-adrenoceptor activated calcium influx. It differs from verapamil and nifedipine by its use dependence. In order for the blockade to occur, the channels must be in the activated state. Diltiazem has no significant affinity for calmodulin. The side effects are headache, edema, and dizziness. 

Antidiabetic Drugs other than Insulin. Figure 1 Sulphonylureas stimulate insulin release by pancreatic (3-cells. They bind to the sulphonylurea receptor (SUR-1), which closes Kir6.2 (ATP-sensitive) potassium channels. This promotes depolarisation, voltage-dependent calcium influx, and activation of calcium-sensitive proteins that control exocytotic release of insulin. 

Although, to our knowledge, the effects of inhalation of amyl nitrite or butyl nitrite on glutamatergic neurotransmission have not been studied, NO, the potent compound that mediates the peripheral effects of nitrites in blood vessels, if released in the CNS when nitrites are inhaled, may potentially affect the glutamatergic system. NO has been reported to act directly on the postsynaptic NMDA receptor, where it can increase or decrease NMDA-mediated currents and subsequent calcium influx (Aizenman et al. 1990 Dingledine et al. 1999 Manzoni et al. 1992). 

Liu PS, Kao LS, Lin MK. 1994. Organophosphates inhibit catecholamine secretion and calcium influx in bovine adrenal chromaffin cell. Toxicology 90 81-91. 

Decreased cerebral blood flow, resulting from acute arterial occlusion, reduces oxygen and glucose delivery to brain tissue with subsequent lactic acid production, blood-brain barrier breakdown, inflammation, sodium and calcium pump dysfunction, glutamate release, intracellular calcium influx, free-radical generation, and finally membrane and nucleic acid breakdown and cell death. The degree of cerebral blood flow reduction following arterial occlusion is not uniform. Tissue at the... 

Calcium influx Immune Teleost fish — Increased Burnett (1997)... 

If some of the electrophysiological effects of oxidant stress occur secondary to an elevation in intracellular calcium, it is important to consider the possible factors that may underlie the initial elevation of calcium. In the simplest analysis, elevation of cytosolic calcium may be due to (1) redistribution of intracellular calcium stores (2) increased calcium influx or (3) decreased calcium efflux. 

Coetzee and Opie (1988, 1992) have suggested that the cellular calcium overload induced by oxidant stress is mediated by an increase in calcium influx through the L-type calcium channel. However, a number of other studies, using different radical-generating systems, experimental conditions and species, have described no significant effects on the calcium channel over the period of exposure necessary to induce cellular calcium overload (Bhatnagar etal., 1990 Shattock etal., 1990 Beresewicz... 

A sustained inhibition of the Na/K pump following a period of oxidant stress would be expected to raise intracellular sodium and favour calcium influx via the Na/Ca exchanger. Ischaemia and reperflision-induced oxidant stress, therefore, may result in a loss of Na/K pump activity, an eflFect that may involve free-radical-mediated changes in cellular thiol status. 

During ischaemia, NOS is activated by calcium influx or by cytokines like tumour necrosis factor (TNF) or by lipopolysaccharide (LPS) and NO is produced in excess. It has been proposed that the excitotoxic effect of glutamate, which contributes to ischaemia-induced neuronal damage, is mediated by increased production of NO via a chain of events that includes increases in intracellular calcium (via glutamate activation of NMDA receptors), calcium activation of NOS, production of NO and peroxynitrite, and induction of lipid peroxidation. In fact, N-nitro-L-atginine, a selective inhibitor of NOS, has been shown to prevent glutamate-induced neurotoxicity in cortical cell cultures (Dawson rf /., 1991). 

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