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<title>VASCUMIT - Comunicaciones a congresos, conferencias, etc.</title>
<link>https://uvadoc.uva.es/handle/10324/43680</link>
<description/>
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<rdf:li rdf:resource="https://uvadoc.uva.es/handle/10324/25024"/>
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<dc:date>2026-04-14T15:29:38Z</dc:date>
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<item rdf:about="https://uvadoc.uva.es/handle/10324/25024">
<title>Calcium signalling in cardiac muscle cells</title>
<link>https://uvadoc.uva.es/handle/10324/25024</link>
<description>In heart cells, severa! distinct kinds of transient spatial patterns of cytoplasmic calcium ion concentration ([ Ca2 + )¡) can be observed: (1) [ Ca2 + )¡ waves, in which regions of spontaneously increased [ Ca2 + ] ; propagate at high velocity (100 ¡.im/s) through the cell; (2) Ca2 + 'sparks', which are spontaneous, non-propagating changes in [ Ca2 + ] ; that are localized in small ( == 2 ¡.im) subcellular regions; and (3) evoked [ Ca2 + )¡ transients that are elicited by electrical  depolarization,  in  association  with  normal  excitation-contraction   (E­&#13;
C) coupling. In confocal [ Ca2 + ] ¡ images, evoked [ Ca2 + ] ; transients appear to be nearly spatially uniform throughout the cell, except during their rising phase or during small depolarizations. In contrast to [Ca2 + )¡ waves and spontaneous Ca2 + sparks, evoked [ Ca2 + ] ; transients are triggered by L-type Ca2 + channel current and they are 'controlled', in the sense that stopping the L-type Ca2 + current stops them. Despite their different characteristics, ali three types of Ca2 + transient involve Ca2 + -induced release of Ca2 + from the sarcoplasmic reticulum. Here, we address the question of how the autocatalytic process of Ca2 + -induced Ca2 + release, which can easily be understood to underlie spontaneous regenerative ('uncontrolled'), propagating [Ca2 + )¡ waves, might be 'harnessed', under other circumstances, to produce controlled changes in [ Ca2 + ]¡, as during normal excitation-contraction coupling, or changes in [ Ca2 + )¡ that do not propagate. We discuss our observations of Ca2 + waves, Ca2 + sparks and normal Ca2 + transients in heart cells and review our results on the 'gain' of Ca2 + -induced Ca2 + release. We discuss a model involving Ca2 + microdomains beneath L-type Ca2 + channels, and clusters of Ca2 + -activated Ca2 + release channels in the sarcoplasmic reticulum which may form the basis of the answer to this question
</description>
<dc:date>1995-01-01T00:00:00Z</dc:date>
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