title: K(ATP) channel current increases in postinfarction remodeled cardiomyocytes.
abstract: Adenosintriphosphate-sensitive potassium channels (K(ATP) channels) are an important linkage between the metabolic state of a cell and electrophysiological membrane properties. In this study, K(ATP) channels were studied in myocytes of normal and remodeled myocardium of the rat. Myocardial infarction was induced by ligature of the left anterior descending artery. Remodeled myocytes were obtained from the hypertrophied posterior left ventricular wall and interventricular septum 3 months after infarction. The current through K(ATP) channels was measured in whole-cell and inside-out patches by using the patch-clamp technique. After myocardial infarction, the heart weight/body weight ratio was doubled and the myocytes were hypertrophied yielding a cell capacitance of 266+/-16 pF compared to 122+/-12 pF in control cells. The amount of Kir6.2 protein was indistinguishable in corresponding regions of control and remodeled hearts. The ATP sensitivity of K(ATP) channels in remodeled cells was significantly lower than in control cells (half maximum block at 115 micromol/l ATP in remodeled and at 71 mumol/l ATP in control cells). The maximum I (KATP) density induced by metabolic inhibition was higher in small remodeled (176+/-15 pA/pF) than in control cells (127+/-11 pA/pF), but was unchanged in large remodeled cells. Both, the higher I (KATP) density and the lower sensitivity of the K(ATP) channels to ATP suggest that remodeled cardiomyocytes develop an improved tolerance to ischemia by stabilizing the resting potential and decreasing excitability.
authors.affiliation: Department Internal Medicine I, Friedrich Schiller University Jena, Erlanger Allee 101, 07740, Jena, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Surber
authors.forename: C
authors.initials: C
authors.lastname: Bollensdorff
authors.forename: S
authors.initials: S
authors.lastname: Betge
authors.forename: T
authors.initials: T
authors.lastname: Zimmer
authors.forename: K
authors.initials: K
authors.lastname: Benndorf
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D002478:Cells, Cultured; D005260:Female; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology*; D015640:Ion Channel Gating; D008564:Membrane Potentials; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D032383:Myocytes, Cardiac / Q000378:metabolism*; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D011917:Rats, Inbred Lew; D020257:Ventricular Remodeling
chemical_list: D015221:Potassium Channels; C117780:mitochondrial K(ATP) channel