Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cellular Ca balance and the dynamic Ca fluxes which occur during each cardiac cycle are complicated by numerous and interdependent different Ca transport systems and binding sites in cardiac myocytes. Since alterations in cellular Ca regulation can be crucial determinants of cardiac dysfunction (both mechanical and arrhythmogenic), it is important to have a fairly clear and somewhat quantitative fundamental understanding of how these systems interact in the intact ventricular myocyte. Several different methods are described for the measurement of Ca fluxes in cardiac myocytes: Ca electrodes, voltage/patch clamp, and fluorescent indicators. With these tools, the roles of Ca entry via Ca current and Na/Ca exchange and sarcoplasmic reticulum (SR) Ca release are discussed in terms of the activation of contraction. The relative roles of Ca removal during relaxation via the SR Ca-adenosine triphosphatase (ATPase), Na/Ca exchange, sarcolemmal Ca-ATPase, and mitochondrial uniporter are also evaluated quantitatively (with the first two being dominant). There are also significant species-dependent differences in the Ca fluxes (where the SR Ca-ATPase is stronger in rat than rabbit and the converse is true for the Na/Ca exchange). There are even differences in the direction of net Ca transport across the cell membrane during the cardiac cycle. In the steady state, it is also clear that the amount of Ca which enters the cell during each cycle must equal the amount extruded from the cell in order to maintain a steady state and prevent progressive Ca overload or loss. In this context, it appears that the amount of Ca which enters the cell via Ca current during the action potential is extruded via Na/Ca exchange during contraction and relaxation.
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PMID:Measurement of calcium transport in heart using modern approaches. 868 74