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Intracellular Ca2 waves

What is the role of intracellular Ca2+ waves due to Ca2+ release from the SR In many cell types stimulation results in Ca2+ waves rather than a maintained increase of [Ca2+] . Summation of such waves in many cells can result in a maintained contraction. Indeed, recent work suggests that these waves are implicated in the genesis of vascular tone (Peng et al 2001). It is important for us to consider how widespread in smooth muscle excitation-contraction coupling are such waves. [Pg.2]

Since the first report by lino and co-workers in 1994 (lino Tsukioka 1994), asynchronous wave-like [Ca2+]j oscillations have emerged as an universal mode of Ca2+ signalling in in situ VSMCs (Table 1). Confocal microscopy of intracellular Ca2+-sensitive dyes in intact blood vessels, reveals recurrent intracellular Ca2+ waves travelling through the longitudinal axis of the ribbonshaped VSMCs. These waves, which are usually but not always initiated by agonists, do not propagate between cells. [Pg.28]

Intracellular Ca2+ waves have been described in a number of cell types. Intracellular Ca2+ waves are expressed in the absence of Ca2+, therefore stored intracellular Ca2+ must be one source of the Ca2+ responsible for the Ca2+ wave. Early work in Xenopus oocytes demonstrated that Ca2+ waves can be observed with expression of only ryanodine receptors (Clapham et al 1993). [Pg.175]

Intracellular Ca2+ waves have been observed both in the absence of Ca2+ in the bathing solution and in the presence of non-specific blockers of transmembrane Ca2+ entry, such as La3+. Thus, the primary source of Ca2+ for intracellular Ca2+ waves is intracellular, specifically the SR Ca2+ stores. In human myocytes, these stores can be visualized (Young Mathur 1999) using the low-affinity Ca2+-dependent fluorescent dye Fluo-3-FF (Fig. 2). Interestingly, the Ca2+ stores... [Pg.177]

An intracellular Ca2+ wave in one cell can initiate an intracellular Ca2+ wave in an adjacent cell. This wave that crosses cell boundaries is then termed an i /i rcellular Ca2+ wave. Two distinctly different mechanisms appear likely for this process gap junctional (Paemeleire et al 2000) or paracrine (Young Hession 1997). It is the ability of Ca2+ waves to communicate relatively slowly (5 to 30 tm/s) over short ranges (hundreds of microns) that distinguishes them from action potential... [Pg.180]

In summary, cultured human myocytes exhibit intracellular Ca2+ waves that may assist with communication within and between adjacent cells. The primary mechanism of intracellular Ca2+ wave propagation is regenerative release of intracellular SR Ca2+ stores through ryanodine or InsP3 receptors, or both together (Fig. 4). As such, the SR Ca2+ store/release system can be considered to... [Pg.181]

Young That is what we are trying to do now, in whole tissue. I have done some of these experiments and the only thing I can really say is that the intracellular Ca2+ waves are generally the same as they are in cultured cells. [Pg.186]

Young In any calculation you allow for a number of variables in terms of trying to model the system of action potential propagation. We know that action potentials have to travel within a fasciculus, which is a macroscopic 1—2 mm connective tissue grouping of bundles. Those do not follow a very tortuous route, at the most they wind once or twice over 30 cm, but not much larger than that. The best simulation that s been done using action potential alone used around nine parameters and was totally unrealistic. I probably didn t point it out but the dashed line that overlayed my clinical contraction was where I actually assumed a 350 /tm size bundle. I assumed an intracellular Ca2+ wave and cell activity for 20 s, and I was able to fit it except for the foot at the end (Young 1997). [Pg.187]

Young In the myometrium, the Ca2+ waves are from the deep cytoplasmic Ca2+ to the plasma membrane. The intracellular Ca2+ waves should be considered separately from either phasic or tonic smooth muscle types. The myometrium is phasic smooth muscle. And intercellular Ca2+ waves are an entirely different phenomenon altogether. [Pg.273]

Local and transient Ca2+ increases that propagate throughout the cytosol of individual cells in the form of waves. Ca2+ waves are generated by a positive feedback activation of Ca2+ release from the intracellular Ca2+ stores through ryanodine receptors or inositol IP3 receptors. [Pg.306]

The general mechanism of Ca2+ wave propagation is believed to be as follows. An event occurs that results in a small rise of intracellular Ca2+ near an SR release receptor (either ryanodine receptor or inositol-1,4,5-trisphosphate [InsPs] receptor). The release of SR Ca2+ results in a local increase of cytoplasmic Ca2+. The nascent cytoplasmic Ca2+ then diffuses to adjacent release sites, causing further SR release. This process is a regenerative process and will remain so as long as the receptors are functional and the SR Ca2+ stores are sufficient. The Ca2+ wave can then be envisioned as a series of SR Ca2+ release events that are dependent upon local Ca2+ concentrations, receptor function, receptor density and diffusion of cytoplasmic Ca2+. The rate of propagation of the Ca2+ wave is possibly dependent upon any of these processes. [Pg.175]

Since Ca2+ waves are rises of intracellular free Ca2+, Ca2+ imaging is required to visualize them. Generally fast, high-affinity Ca2+-sensitive fluorescent dyes such... [Pg.175]

Young I can explain ATP. I did these experiments looking at intercellular Ca2+ waves and apyrase, and there is no effect. It turns out that the presence of either a prostaglandin transporter blocker, which is the same class as a Cl channel blocker, or a prostaglandin synthesis inhibitor, interrupts intracellular Ca2+ that is far away. It does not interrupt the intercellular Ca2+ through the gap junctions there are two different mechanisms. [Pg.184]

Kotlikoff I have a question about InsP3 receptors and ryanodine receptors. There is good evidence for wave propagation with both systems in smooth muscle. Can you say anything in experiments where you have looked with antibodies about the relationship between InsP3 receptors and ryanodine receptors And does this provide any insight into the interaction between these Ca2+-sensitive intracellular Ca2+ release channels ... [Pg.269]

Influx of Ca2+ through a-LTX pores might explain Ca2+-dependent secretion, but not the bursts of miniatures. These may be due to Ca2+ waves caused by activation of phospholipase C (PLC) (Vicentini and Meldolesi 1984 Davletov et al. 1998) and release of intracellular Ca2+ (Ca2+,). In fact, U73122 (blocks PLC activation by G proteins), thapsigargin (depletes Ca2+ stores), and 2-APB (inhibits activation of Ca2+ stores) block a-LTX action (Davletov et al. 1998 Ashton et al. 2001 Capogna et al. 2003), impheating a G protein cascade in Ca2+-dependent toxin-induced release. [Pg.175]


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