Background Sodium-calcium (Ca) exchanger isoform 1 (NCX1) is the dominant Ca efflux mechanism in cardiomyocytes and is critical to maintaining Ca homeostasis during excitation-contraction coupling. NCX1 activity has been implicated in the pathogenesis of cardiovascular diseases, but a lack of specific NCX1 blockers complicates experimental interpretation. Our aim was to develop a tamoxifen-inducible NCX1 knockout (KO) mouse to investigate compensatory adaptations of acute ablation of NCX1 on excitation-contraction coupling and intracellular Ca regulation, and to examine whether acute KO of NCX1 confers resistance to triggered arrhythmia and ischemia/reperfusion injury.
View Article and Find Full Text PDFNa/Ca exchange is the dominant calcium (Ca) efflux mechanism in cardiac myocytes. Although our knowledge of exchanger function (NCX1 in the heart) was originally established using biochemical and electrophysiological tools such as cardiac sarcolemmal vesicles and the giant patch technique [1-4], many advances in our understanding of the physiological/pathophysiological roles of NCX1 in the heart have been obtained using a suite of genetically modified mice. Early mouse studies focused on modification of expression levels of NCX1 in the ventricles, with transgenic overexpressors, global NCX1 knockout (KO) mice (which were embryonic lethal if homozygous), and finally ventricular-specific NCX1 KO [5-12].
View Article and Find Full Text PDFObjectives: Pregnant women routinely receive information in support of or opposing infant immunization. We aimed to describe immunization information sources of future mothers' and determine if receiving immunization information is associated with infant immunization timeliness.
Methods: We analyzed data from a child cohort born 2009-2010 in New Zealand.
Transverse-axial tubules (TATs) are commonly assumed to be sparse or absent in atrial myocytes from small animals. Atrial myocytes from rats, cats and rabbits lack TATs, which results in a characteristic "V"-shaped Ca release pattern in confocal line-scan recordings due to the delayed rise of Ca in the center of the cell. To examine TAT expression in isolated mouse atrial myocytes, we loaded them with the membrane dye Di-4-ANEPPS to label TATs.
View Article and Find Full Text PDFKey Points: Repolarizing currents through K channels are essential for proper sinoatrial node (SAN) pacemaking, but the influence of intracellular Ca on repolarization in the SAN is uncertain. We identified all three isoforms of Ca -activated small conductance K (SK) channels in the murine SAN. SK channel blockade slows repolarization and subsequent depolarization of SAN cells.
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