Electrophysiological Studies of Wild-Type and Mutant Na+-Ca2+ Exchange Proteins
In cardiac muscle, Na+-Ca2+ exchange is the primary mechanism for transsarcolemmal Ca2+ efflux (for reviews, see [1–3]). The majority of Ca2+ entering through L-type Ca2+ channels during the action potential is removed by this mechanism [4,5]. Recently, it has been postulated that Na+-Ca2+ exchange may also play a role in the Ca2+-induced Ca2+-release mechanism during cardiac contractions [6–8]. That is, Ca2+ entry through reverse Na+-Ca2+ exchange may trigger an additional release of Ca2+ from the sarcoplasmic reticulum. Although the contribution of this mechanism to physiological excitation-contraction coupling has not been unequivocally established [9–11], this postulation raises the possibility that Na+-Ca2+ exchange plays a prominent role in both contraction and relaxation of cardiac muscle.
KeywordsXenopus Oocyte Exchange Current Exchange Protein Niflumic Acid Transport Site
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