Intracellular calcium release, effect

Theophylline may also act as an adenosine antagonist.86 113 Adenosine is thought to bind to specific receptors on the smooth-muscle cells and to stimulate contraction. By blocking this effect, theophylline would facilitate smooth-muscle relaxation. Theophylline may likewise help produce bronchodilation by other mechanisms, such as inhibition of intracellular calcium release and stimulation of catecholamine release.115 In reality, theophylline and similar drugs may induce bronchodilation and help protect the airways through a combination of several mechanisms, but the relative importance of each cellular effect remains to be determined. 

In primary cerebellar cultures and acutely isolated cerebellar granule neurons, methanandamide has been demonstrated to enhance NMDA-evoked calcium release (Netzeband et al., 1999). This effect was due to activation of the CB, receptor. In a smdy using inhibitors of VDCC, a variety of compounds known to modulate intracellular calcium release, and PKC and PKA inhibitors, it was determined that the enhancement of NMDA-evoked calcium release was due to CB,-receptor activation of the phospholipase C pathway this led to the downstream release of calcium from intracellular stores. In this study, it was also noted that blockade of the phospholipase C pathway unmasked a CB,-mediated inhibition of the NMDA-evoked calcium release (Netzeband et al., 1999). This is consistent with the study reported by Hampson et al. (1998) in rat brain shces, referred to earlier. 

Wu S et al. (2001) Cardiac effects of the extract and active components of Radix stephaniae tetrandrae. I. Electrically induced intracellular calcium transient and protein release during the calcium paradox. Life Sci 68(25) 2853-2861... 

However, the current view of the regulation of calcium ion entry into the cytoplasm by PLC-linked stimuli holds that activation occurs not as a direct result of the action of IP3 on the plasma membrane but indirectly, as a result of depletion of calcium ions from an intracellular store by IP3 [14]. In the context of this capacitative model , the actions of intracellularly applied IP3 and heparin reflect the effects of these maneuvers on intracellular release process from ER into cytosol, rather than via the plasma membrane. The reported actions of I(1,3,4,5)P4, if in fact they do represent physiological control mechanisms, may reflect an ability of I(1,3,4,5)P4 to augment the calcium-releasing ability of IP3, rather than a distinct and... 

On the other hand, mercuric chloride decreased both spontaneous and evoked transmitter liberation at the frog neuromuscular junction [98] as well as the release of vasopressin from the pituitary gland [99] it was suggested that these effects are mediated via changes in the intracellular calcium ion concentration. 

While ionophore-stimulated 5-LO product release from neutrophils is often used as an indication of 5-LO inhibition, one must interpret these results cautiously. For example, halothane, an inhalation anaesthetic which may cause membrane perturbation [26], and colchicine, a microtubule disrupter [27], both were active, but presumably not because of 5-LO inhibition. A23187 is assumed to stimulate 5-LO by raising the intracellular calcium level, but this agent causes many other effects which may or may not be related to 5-LO activation, including changes in membrane potential, protein phosphorylation, phospholipid turnover, cyclic nucleotide levels, and DNA and protein synthesis [28]. Also, the effects of some putative 5-LO inhibitors on product release from neutrophils has been shown to vary with the stimulant used [29]. 

In addition to participating in the activation of PKC, calcium released from intracellular organelles has several other effects on cellular processes. Most of these actions are mediated through the protein calmodulin (CaM). Calmodulin has no activity in and of itself, but in the Ca -bound state, serves to modulate the activity of several other proteins, including some forms of ad-... 

Three subtypes of vasopressin G protein-coupled receptors have been identified. Via receptors mediate the vasoconstrictor action of vasopressin V , receptors potentiate the release of ACTH by pituitary corticotropes and V 2 receptors mediate the antidiuretic action. Via effects are mediated by activation of phospholipase C, formation of inositol trisphosphate, and increased intracellular calcium concentration. V2 effects are mediated by activation of adenylyl cyclase. 

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