title: Regional gradation of L-type calcium currents in the feline heart with a healed myocardial infarct.
abstract: BACKGROUND
  Abnormal action potentials in myocytes adjacent to > 2-month-old feline LV myocardial infarcts (MI) may reflect alterations in Ca2+ currents (Ica).
  
  
  RESULTS
  We compared ICa, at 36 degrees C, in subendocardial myocytes isolated from areas adjacent to MI and to ICa in cells from remote areas (> 4 mm away; REM) and control cells from similar regions in normal hearts. Control (CON) myocytes had membrane capacitance of 234 +/- 10 pF (n = 81 cells) compared to 305 +/- 14 pF in REM (71 cells; P < 0.05 from CON) and 237 +/- 11 pF (n = 55 cells) in MI (not different from CON). From Vh = -40 mV; peak ICa elicited by test potentials (-35 to +70 mV) were significantly larger in CON (-1746 +/- 123 pA) and REM (-1795 +/- 142 pA) compared to MI (-1352 +/- 129 pA) (P < 0.05). Peak ICa density was significantly reduced in REM (-6.0 +/- 0.4 pA/pF) or MI (-5.7 +/- 0.4 pA/pF, P < 0.05) compared to CON (-7.5 +/- 0.4 pA/pF). Double exponential ICa decay was similar among groups. Half-inactivation potential (V0.5) was significantly shifted (hyperpolarizing direction) for MI (-29.1 +/- 2.6 mV) and REM (-24.6 +/- 1.2 mV) myocytes compared to -20.3 +/- 1.0 mV in CON. MI slope factor (k; 9.0 +/- 0.5) was significantly different from CON (6.8 +/- 0.3) and REM (7.3 +/- 0.4). No differences in time course of recovery from inactivation were noted. Five millimolar Ba2+o produced significant increases in ICa in CON and REM but an attenuated response in MI. Bay K8644 (1 microM) produced similar ICa increase in all groups. ICa increase due to isoproterenol (1 microM) in MI and REM was half that in CON, but there were no differences in increased ICa responses among groups following phenylephrine (10 microM).
  
  
  CONCLUSIONS
  Reduced ICa density in REM reflects cell hypertrophy, whereas altered ICa of MI may reflect altered channel structure and/or function.
authors.affiliation: Department of Medicine, University of Miami School of Medicine, Florida 33101-6189, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: Pinto
authors.forename: F
authors.initials: F
authors.lastname: Yuan
authors.forename: B J
authors.initials: BJ
authors.lastname: Wasserlauf
authors.forename: A L
authors.initials: AL
authors.lastname: Bassett
authors.forename: R J
authors.initials: RJ
authors.lastname: Myerburg
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D002415:Cats; D004594:Electrophysiology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D007700:Kinetics; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D018924:Vascular Capacitance / Q000187:drug effects / Q000502:physiology
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels