title: Spatial alterations of Kv channels expression and K(+) currents in post-MI remodeled rat heart.
abstract: OBJECTIVE
  The hypothesis being tested in the present study is that increased anisotropic properties occurs in the remodeled post-infarction heart due to spatial alterations in Kv channels expression and K(+) currents of the remodeled myocardium.
  
  
  METHODS
  Three to 4 weeks post myocardial infarction (MI) in the rat, we measured the two components of the outward K(+) current, I(to-fast (f)) and I(to-slow(s)) in the epicardium (epi) and endocardium (endo) of noninfarcted remodeled left ventricle (LV) using patch clamp techniques. Alterations in mRNA and/or protein levels of potassium channel genes Kv1.4, Kv1.5, Kv2.1, Kv4.2 and Kv4.3 were measured in epi, midmyocardium (mid), and endo regions of LV and in the right ventricle (RV).
  
  
  RESULTS
  In sham operated rat heart, the density of I(to-f) was 2.3 times greater in epi compared to endo myocytes. In post-MI heart, the density of I(to-f) and I(to-s) decreased to a similar degree in LV epi and endo but the difference in I(to-f) density between epi and endo persisted. The mRNA and/or protein levels of Kv1.4, Kv2.1, Kv4.2 and Kv4.3 but not Kv1.5 decreased to a varying extent in different regions of LV but not in RV of post-MI heart.
  
  
  CONCLUSIONS
  Our results suggest that regional downregulation of Kv channels expression and density of K(+) currents can be a significant determinant of increased spatial electrophysiological heterogeneity and contribute to increased electrical instability of the post-MI heart.
authors.affiliation: Cardiology Division, Department of Medicine, Box 1199, State University of New York Health Science Center and Veterans Affairs Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.
authors.forename: B
authors.initials: B
authors.lastname: Huang
authors.forename: D
authors.initials: D
authors.lastname: Qin
authors.forename: N
authors.initials: N
authors.lastname: El-Sherif
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western / Q000379:methods; D051668:Delayed Rectifier Potassium Channels; D004699:Endocardium / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D051665:Kv1.4 Potassium Channel; D051666:Kv1.5 Potassium Channel; D023421:Models, Animal; D009203:Myocardial Infarction / Q000378:metabolism / Q000503:physiopathology*; D018408:Patch-Clamp Techniques; D010496:Pericardium / Q000378:metabolism; D015221:Potassium Channels / Q000032:analysis / Q000235:genetics* / Q000378:metabolism; D024642:Potassium Channels, Voltage-Gated; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D051669:Shab Potassium Channels; D051672:Shal Potassium Channels; D000254:Sodium-Potassium-Exchanging ATPase; D020257:Ventricular Remodeling
chemical_list: D051668:Delayed Rectifier Potassium Channels; C496979:Kcna4 protein, rat; C496983:Kcna5 protein, rat; C496991:Kcnb1 protein, rat; C497023:Kcnd3 protein, rat; D051665:Kv1.4 Potassium Channel; D051666:Kv1.5 Potassium Channel; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D012333:RNA, Messenger; D051669:Shab Potassium Channels; D051672:Shal Potassium Channels; D000254:Sodium-Potassium-Exchanging ATPase