Calcium release induced

Mechanism of Action A bisphosphonate that inhibits the resorption of mineralized bone and cartilage inhibits increased osteoclastic activity and skeletal calcium release induced by stimulatory factors produced by tumors. Therapeutic Effect Increases urinary calcium and phosphorus excretion decreases serum calcium and phosphorus levels. 

It has been reported that D1 receptor stimulation can induce an intracellular mobilization of Ca2+ via the interaction of D1 receptor with a novel protein, calcyon (Lezcano et al., 2000). By a two-hybrid screening in yeast, calcyon was shown to associate with the C-terminal tail of D1 and D5 receptor. Activation of PKC by various stimulants allowed calcyon to couple the D1 or possibly D5 receptors with Gq protein, rendering these receptors able to produce intracellular Ca2+ mobilization. Calcyon is expressed at higher levels in the cortex than in the striatum and the intracellular calcium release induced by D1/D5 receptor stimulation is detected in cortical and hippocampal neurons in culture, but not in striatal neurons (Lezcano and Bergson, 2002 Zelenin et al., 2002). 

Komori, S. and Bolton, T.B. (1991) Calcium release induced by inositol 1,4,5-trisphosphate in sin e rabbit intestinal smooth muscle cells. Journal of Physiology (London), 433 495-517. 

Meyer, T. L. Stryer. 1990. Transient calcium release induced by successive increments of inositol 1,4,5-trisphosphate. Proc. Natl. Acad. Sci. USA 87 3841-5. 

Dayanithi G, Yahi N, Baghdlguian S, Fantini J. Intracellular calcium release induced by human immunodeficiency virus type 1 (HlV-1) surface envelope glycoprotein in human intestinal epithelial cells a putative mechanism for HlV-1 enteropathy. Cell Calcium. 1995 18(1) 9-18. 

The NHR contains also the conserved Calcineurin docking site, PxlxIT, required for the physical interaction of NEAT and Calcineurin. Dephosphorylation of at least 13 serines residues in the NHR induces a conformational change that exposes the nuclear localization sequences (NLS), allowing the nuclear translocation of NEAT. Rephosphorylation of these residues unmasks the nuclear export sequences that direct transport back to the cytoplasm. Engagement of receptors such as the antigen receptors in T and B cells is coupled to phospholipase C activation and subsequent production of inositol triphosphate. Increased levels of inositol triphosphate lead to the initial release of intracellular stores of calcium. This early increase of calcium induces opening of the plasma membrane calcium-released-activated-calcium (CRAC) channels,... 

However, the total regulatory system is not so simple and linear. In skinned muscle preparations especially, it can be shown that there are calcium stores which cannot be released by IP3 but which are released by elevated levels of calcium itself That is, by the mechanism of calcium induced calcium release (CICR). The CICR... 

Trimm, J.L., Salama, G. and Abramson, J.J. (1986). Sulphydryl oxidation induces rapid calcium release from sarcoplasmic reticulum vesicles. J. Biol. Chem. 261, 16092-16098. 

McGrath J, Solter D 1984 Inability of mouse blastomere nuclei transferred to enucleated zygotes to support development invitro. Science 226 1317-1319 Miyazaki S 1988 Inositol 1,4,5-trisphosphate-induced calcium release and guanine nucleotidebinding protein-mediated periodic calcium rises in golden hamster eggs. J Cell Biol 106 345-353... 

In addition to the well-known iron effects on peroxidative processes, there are also other mechanisms of iron-initiated free radical damage, one of them, the effect of iron ions on calcium metabolism. It has been shown that an increase in free cytosolic calcium may affect cellular redox balance. Stoyanovsky and Cederbaum [174] showed that in the presence of NADPH or ascorbic acid iron ions induced calcium release from liver microsomes. Calcium release occurred only under aerobic conditions and was inhibited by antioxidants Trolox C, glutathione, and ascorbate. It was suggested that the activation of calcium releasing channels by the redox cycling of iron ions may be an important factor in the stimulation of various hepatic disorders in humans with iron overload. 

The functions of mtNOS in mitochondria have been studied (see Chapter 23). Ghafourifar et al. [177] found that the calcium-induced stimulation of mtNOS caused the release of cytochrome c from mitochondria and induced apoptosis. On the other hand, the same group of authors [178] showed that the production of NO by mtNOS and superoxide in mitochondria resulted in the formation of peroxynitrite and stimulated calcium release, indicating the existence of a feedback loop which prevents calcium overload in mitochondria. 

Collier ML, Ji G, Wang Y, Kotlikoff MI 2000 Calcium-induced calcium release in smooth muscle loose coupling between the action potential and calcium release. J Gen Physiol 115 653-662... 

Ji G, Feldman M, Barsotti RJ, Kotlikoff MI 2002 Stretch-induced calcium release in smooth muscle. J Gen Physiol, in press... 

Finch EA, Turner TJ, Goldin SM 1991 Calcium as a coagonist of inositol 1,4,5-trisphosphate-induced calcium release. Science 252 443-446... 

Somlyo AV, Somlyo AP 1971 Strontium accumulation by sarcoplasmic reticulum and mitochondria in vascular smooth muscle. Science 174 955-958 Somlyo AV, Bond M, Somlyo AP, Scarpa A 1985 Inositol-trisphosphate induced calcium release and contraction in vascular smooth muscle. Proc Natl Acad Sci 82 5231-5235 Somlyo AV, Horiuti K, Trentham DR, Kitazawa T, Somlyo AP 1992 Kinetics of Ca2+ release and contraction induced by photolysis of caged D-myo-inositol 1,4,5-trisphosphate in smooth muscle the effects of heparin, procaine, and adenine nucleotides. J Biol Chem 267 22316-22322... 

Neurotransmitter release induced by potassium-dependent depolarization is a physiologically relevant way to investigate pyrethroid effects on calcium-dependent neurotransmitter release since this process is independent of voltage-sensitive sodium channels [71]. Furthermore, potassium-stimulated calcium influx and subsequent neurotransmitter release by synaptosomes is blocked by a variety of voltage-sensitive calcium channel antagonists but not by TTX [4, 71, 72]. 

Matsumoto M, Inagaki M, Kiuchi Y, et al. 1993. Role of calcium ions in dopamine release induced by sodium cyanide perfusion in rat striatum. Neuropharmacol 32(7) 681-688. 

Mechanism of Action An antihyperglycemic that stimulates release of insulin from beta cells of the pancreas by depolarizing beta cells, leading to an opening of calcium channels. Resulting calcium influx induces insulin secretion. Therapeutic Effect Lowers blood glucose concentration. 

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