title: Atrial cardiomyocyte calcium signalling.
abstract: Whereas Ca(2+) signalling in ventricular cardiomyocytes is well described, much less is known regarding the Ca(2+) signals within atrial cells. This is surprising given that atrial cardiomyocytes make an important contribution to the refilling of ventricles with blood, which enhances the subsequent ejection of blood from the heart. The dependence of cardiac function on the contribution of atria becomes increasingly important with age and exercise. Disruption of the rhythmic beating of atrial cardiomyocytes can lead to life-threatening conditions such as atrial fibrillation. Atrial and ventricular myocytes have many structural and functional similarities. However, one key structural difference, the lack of transverse tubules ("T-tubules") in atrial myocytes, make these two cell types display vastly different calcium patterns in response to electrical excitation. The lack of T-tubules in atrial myocytes means that depolarisation provokes calcium signals that originate around the periphery of the cells. Under resting conditions, such Ca(2+) signals do not propagate towards the centre of the atrial cells and so do not fully engage the contractile machinery. Consequently, contraction of atrial myocytes under resting conditions is modest. However, when atrial myocytes are stimulated with a positive inotropic agonist, such as isoproterenol, the peripheral Ca(2+) signals trigger a global wave of Ca(2+) that propagates in a centripetal manner into the cells. Enhanced centripetal movement of Ca(2+) in atrial myocytes leads to increased contraction and a more substantial contribution to blood pumping. This article is part of a Special Issue entitled: 11th European Symposium on Calcium.
authors.affiliation: Laboratory of Molecular Signalling, The Babraham Institute, Babraham, Cambridge, CB22 3AT, UK. martin.bootman@bbsrc.ac.uk
authors.forename: Martin D
authors.initials: MD
authors.lastname: Bootman
authors.forename: Ioannis
authors.initials: I
authors.lastname: Smyrnias
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Thul
authors.forename: Stephen
authors.initials: S
authors.lastname: Coombes
authors.forename: H Llewelyn
authors.initials: HL
authors.lastname: Roderick
mesh_terms: D000818:Animals; D020013:Calcium Signaling; D056966:Excitation Contraction Coupling; D006325:Heart Atria / Q000166:cytology*; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology; D006352:Heart Ventricles / Q000378:metabolism; D006801:Humans; D032383:Myocytes, Cardiac / Q000378:metabolism*