I K1 and I f in ventricular myocytes isolated from control and hypertrophied rat hearts.
Electrophysiological properties of inward rectifier potassium current (I (K1)) and hyperpolarization-activated inward current (I (f)) and the protein expression of the Kir2.1 subfamily and the hyperpolarization-activated cation channel 2 (HCN2) and HCN4 were studied in control and hypertrophied myocytes. Electrophysiological experiments were conducted by whole-cell patch-clamp technique, and protein levels of Kir2.1 subfamily and HCN2 and HCN4 isoforms were analysed by Western blot technique. The density of I (f) as well as the protein expression levels of the HCN2 isoform was found to be significantly higher in hypertrophied myocytes, whereas the protein expression level of HCN4 was not detected in any group. I (K1) density and Kir 2.1 protein expression were similar in control and hypertrophied myocytes, but the time-course of the currents was slower in hypertrophied myocytes. Analysis of I (f) and I (K1) in the same control and hypertrophied myocyte at -80 mV showed that cells in which I (f) was present had values of I (K1) density similar to those cells in which I (f) was not observed. In conclusion, although left ventricular hypertrophy involves an up-regulation of I (f) and its molecular correlate HCN2 in the rat ventricle, its contribution to diastolic depolarization would be limited by the low values of I (f) density at potentials close to the resting potential of the ventricular cells.
Fernández-Velasco
María
M
Institute of Pharmacology and Toxicology (CSIC-UCM), School of Medicine, Universidad Complutense, 28040 Madrid, Spain.
Ruiz-Hurtado
Gema
G
Delgado
Carmen
C
D000818:Animals; D004594:Electrophysiology; D015870:Gene Expression; D006352:Heart Ventricles / Q000378:metabolism; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism* / Q000473:pathology; D007473:Ion Channels / Q000378:metabolism*; D008297:Male; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D020033:Protein Isoforms / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
C513836:HCN4 protein, rat; C578712:Hcn2 protein, rat; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D007473:Ion Channels; C489461:Kir2.1 channel; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D020033:Protein Isoforms; D011188:Potassium