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  • Title: Electrical remodeling of membrane ionic channels of hypertrophied ventricular myocytes from spontaneously hypertensive rats.
    Author: Li X, Jiang W.
    Journal: Chin Med J (Engl); 2000 Jul; 113(7):584-7. PubMed ID: 11776022.
    Abstract:
    OBJECTIVE: To study the difference in membrane ionic currents between hypertrophied and normal myocytes and to explore the electrical remodeling of hypertrophied myocytes. METHODS: Membrane ionic channels were studied in enzymatically dispersed spontaneously hypertensive rats (SHRs) left ventricular myocytes using the whole-cell configuration of patch-clamp technique, with normal Wistar rats ventricular myocytes as controls. We observed depolarizing currents (sodium current, INa; L-type calcium current, L-ICa) and repolarizing currents (inward rectifier potassium current, IK1; delayed rectifier potassium current, IK; transient outward potassium current, Ito) and compared the differences between normal and hypertrophied myocytes. RESULTS: The heart to body weight ratio of Wistar rats and SHRs was 3.70 +/- 0.29 mg/g and 5.66 +/- 0.46 mg/g, respectively (P < 0.001), and the mean cell membrane capacitances were 189.94 +/- 56.59 pF and 280.68 +/- 67.98 pF, respectively (P < 0.05). These differences suggest that SHRs have heart hypertrophy and hypertrophied myocytes. The amplitude of L-Ica of SHRs (1944 +/- 466.8 pA) was significantly greater than that of Wistar rats (1136 +/- 383.3 pA) (P < 0.001), and the current density was 6.93 +/- 1.71 pA/pF and 6.19 +/- 2.85 pA/pF respectively when normalized to cell capacitance, and the slow inactivation time constant of SHRs was significantly prolonged (56.01 +/- 13.36 ms vs 43.63 +/- 17.89 ms, P < 0.001). The amplitude of INa of SHRs (6132.5 +/- 1162.9 pA) was significantly greater than that of Wistar rats (3613.9 +/- 794.44 pA) (P < 0.001), but there was no difference when normalized to cell capacitance (24.61 +/- 6.72 pA/pF vs 24.95 +/- 6.99 pA/pF). Channel activation and inactivation time constants were also the same. The amplitude of IK of SHRs (3461.5 +/- 1967.10 pA) was greater than that of Wistar rats (2302.4 +/- 893.72 pA) (P < 0.05), but there was no difference when normalized to cell capacitance (12.38 +/- 5.46 pA/pF vs 11.86 +/- 3.59 pA/pF). The inward portion of IK1 of SHRs was significantly lower than that of Wistar rats (11.3 +/- 2.26 pA/pF vs 14.3 +/- 3.00 pA/pF, P < 0.05), but there was no difference in the outward portion (2.360 +/- 0.86 pA/pF vs 2.957 +/- 1.27 pA/pF). The current density of Ito of SHRs (8.21 +/- 6.64 pA/pF) was significantly lower than that of Wistar rats (19.16 +/- 6.17 pA/pF) (P < 0.001), but channel kinetics were similar, suggesting that the reduction of Ito may result from the decrease in channel number. CONCLUSIONS: Membrane ionic current changes of hypertrophied left ventricular myocytes in SHRs include: 1. there was an increase of L-Ica, INa and Ik, but the current density was similar to that in normal myocytes, indicating that channel numbers increase as the myocytes become hypertrophied; 2. Ito was small in hypertrophied ventricular myocytes and its current density was even smaller, indicating that channel numbers decrease as the myocytes enlarge. The former is recognized as a physiologically compensatory change which does not lead to electrophysiological disturbance; the latter is viewed as pathological change, where the reduction of Ito may lead to a repolarizing delay in myocytes, prolongation of the action potential and the occurrence of arrhythmias because of repolarizing heterogeneity. Therefore, the reduction of Ito in hypertrophied myocytes should be recognized as a significant or substantial change of electrical remodeling.
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