Normal Cardiac Excitation: Generation, Propagation and Coupling to Contraction
Principal Investigator: David Eisner

University: University of Manchester, United Kingdom

Main contributions:

  • study intracellular calcium handling and the relationship of calcium to cardiac excitation and contraction in order to
    • characterize pacemaker mechanisms in SAN cells.
    • define molecular mechanisms of functional remodelling in atrial myocytes and their pharmacological control.

Lab web-page: http://www.medicine.manchester.ac.uk/staff/DavidEisner

Contact: eisner@man.ac.uk

Relevant Publications:

  • Eisner DA, Kashimura T, Venetucci LA & Trafford WA. From the Ryanodine Receptor to Cardiac Arryhtmias. Circ J 2009/73:1561-1567. 
  • Walden AP, Dibb KM & Trafford AW. Differences in intracellular calcium homeostasis between atrial and ventricular myocytes. Journal of Molecular and Cellular Cardiology 2009/46:463-473. 
  • Dibb KM, Clarke JD, Horn MA, Richards MA, Graham MK, Eisner DA & Trafford AW. Characterization of an extensive transverse tubular network in sheep atrial myocytes and its depletion in heart failure. Circ Heart Fail 2009/2:482-489. 
  • Eisner D & Cerbai E. Beating to time: calcium clocks, voltage clocks and cardiac pacemaker activity. Am J Physiol Heart Circ Physiol 2009/296:H561-H562. 
  • Ventucci LL, Trafford AW & Eisner DA. Increasing ryanodine receptor open probability alone does not produce arrhythmogenic Ca waves: threshold SR Ca content is required. Circulation Research 2007/100:105-111.  (Link)
  • Kupittayanant P, Trafford AW, Diaz M & Eisner DA. A mechanism distinct from the L-type Ca current or Na-Ca exchange contributes to Ca entry in rat ventricular myocytes. Cell Calcium 2006/39(5):417-23.  (Link)
  • Ventucci LL, Trafford AW, Diaz ME, O'Neill SC & Eisner DA. Reducing Ryanodine Receptor Open Probability As a Means to Abolish Spontaneous Ca2+ Release and Increase Ca2+ Transient Amplitude in Adult Ventricular Myocytes. Circulation Research 2006/98:1299-1305.  (Link)