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Thu Jul 2

• Effects of pressure overload-induc ed hypertrophy on TTX-sensitive inward currents in guinea pig left ventricle: We investigated the effects of pressure overload hypertrophy on inward sodium (I Na) and calcium currents (I Ca) in single left ventricular myocytes to determine whether changes in these current systems could account for the observed prolongation of the action potential. Hypertrophy was induced by pressure overload caused by banding of the abdominal aorta. Whole-cell patch clamp experiments were used to measure tetrodotoxin (TTX)-sensitiv e inward currents. The main findings were that I Ca density was unchanged whereas I Na density after stepping from ?80 to ?30 mV was decreased by 30% (?9.0 ± 1.16 pA pF?1 in control and ?6.31 ± 0.67 pA pF?1 in hypertrophy, p < 0.05, n= 6). Steady-state activation/ina ctivation variables of I Na, determined by using double-pulse protocols, were similar in control and hypertrophied myocytes, whereas the time course of fast inactivation of I Na was slowed (p < 0.05) in hypertrophied myocytes. In addition, action potential clamp experiments were carried out
• Electrophysiol ogical properties of neonatal rat ventricular myocytes with alpha 1-adrenergic-i nduced hypertrophy -- Gaughan et al. 275 (2): H577 -- AJP - Heart and Circulatory Physiology: The electrophysiol ogy of neonatal rat ventricular myocytes with and without hypertrophy has not been characterized. The alpha 1-adrenergic agonist phenylephrine induced hypertrophy in neonatal rat ventricular myocytes. After 48 h of exposure to 20 µM phenylephrine, cell surface area of hypertrophied myocytes was 44% larger than control. Action potential duration was significantly longer in hypertrophy than in control. There was an increase in L-type Ca2+ current in control after 48 h in culture, but current density was significantly less in hypertrophy (-4.7 ± 0.8 hypertrophy vs. -10.7 ± 1.2 control pA/pF, n = 22, P < 0.05). T-type Ca2+ current density was not different. The alpha -adrenergic antagonist prazosin blocked the hypertrophy and the chronic effect of phenylephrine on L-type Ca2+ current. Transient outward K+ current density was decreased 70% in hypertrophy and was blocked with 4-aminopyridin e. No change in Na+ current density was observed. Staurosporine, a protein kinase C i

Sat Jun 27

• Effects of Heart Disease on Cardiac Ion Current Density Versus Current Amplitude: Important Conceptual Subtleties in the Language of Arrhythmogenic Ion Channel Remodeling -- Nattel 102 (11): 1298 -- Circulation Research: In electrophysiol ogical studies, cellular hypertrophy is often assessed by determining cell capacitance. The lipid bilayer (electrically resistive) cell membrane acts as a capacitor separating the electrically conducting intracellular solution from the conductive extracellular solution. Electric current passes across cardiac cell membranes to charge their capacitance, even when no current traverses ion channels. Capacitance is a function of intrinsic capacitive properties (indicated by the "dielectr ic constant" ), the capacitive (in this case, cell membrane) surface area, and the thickness of the capacitor. The thickness and intrinsic capacitive properties of cell membranes are fairly constant, so the dominant factor determining cell capacitance is the total membrane surface area. Cell size increases with cardiac hypertrophy. Augmented cell size is accompanied by increased cell surface area, therefore inevitably increasing cell capacitance.
• Distinct Cellular and Molecular Mechanisms Underlie Functional Remodeling of Repolarizing K+ Currents With Left Ventricular Hypertrophy -- Marionneau et al. 102 (11): 1406 -- Circulation Research: Unexpectedly, expression of IK,slow channel subunits Kv1.5 and Kv2.1 was increased in TAC LV. Biochemical experiments also demonstrated that, although total protein was unaltered, cell surface expression of TASK1 was increased in TAC LV. Functional changes in repolarizing K+ currents with LVH, therefore, result from distinct cellular (cardiomyocyte enlargement) and molecular (alterations in the numbers of functional channels) mechanisms.
• Electrophysiol ogical remodeling in hypertrophy and heart failure -- Tomaselli and Marbán 42 (2): 270 -- Cardiovascular Research: The failing heart undergoes a complex series of changes in both myocyte and non-myocyte elements. In an attempt to compensate for the reduction in cardiac function the sympathetic nervous (SNS), renin?angioten sin?aldosteron e (RAAS) systems and other neurohumoral mechanisms are activated. The altered signal transduction in heart failure initiates changes
• Changes in Ca2+ Cycling Proteins Underlie Cardiac Action Potential Prolongation in a Pressure-Overl oaded Guinea Pig Model With Cardiac Hypertrophy and Failure -- Ahmmed et al. 86 (5): 558 -- Circulation Research: Ventricular arrhythmias are common in both cardiac hypertrophy and failure; cardiac failure in particular is associated with a significant increase in the risk of sudden cardiac death. We studied the electrophysiol ogic changes in a guinea pig model with aortic banding resulting in cardiac hypertrophy at 4 weeks and progressing to cardiac failure at 8 weeks using whole-cell patch-clamp and biochemical techniques. Action potential durations (APDs) were significantly prolonged in banded animals at 4 and 8 weeks compared with age-matched sham-operated animals. APDs at 50% and 90% repolarization (APD50 and APD90 in ms) were the following: 4 week, banded, 208±51 and 248±49 (n=15); 4 week, sham, 189±68 and 213±69 (n=16); 8 week, banded, 197±40 and 226±40 (n=21); and 8 week, sham, 156±42 and 189±45 (n=22), respectively; P<0.05 comparing banded versus sham-operated animals.
• Myocardial Connexin43 Expression in Left Ventricular Hypertrophy Resulting from Aortic Regurgitation: This disease duration-relat ed increase differs from the long-term decrease in connexin43 expression associated with other forms of heart disease and suggests that alterations in connexin expression may play a role in the rhythm abnormalities commonly seen in AR.

Fri Jun 26

• Reduced content of connexin43 gap junctions in ventricular myocardium from hypertrophied and ischemic human hearts -- Peters et al. 88 (3): 864 -- Circulation: Gap junctions in normal adult human working ventricular myocardium occupy an area of 0.0051 micron2/micron 3 myocyte volume. This surface area is reduced in ventricular myocardium from hearts subject to chronic hypertrophy and ischemia, despite a normal number of intercellular abutments, and this alteration may contribute to abnormal impulse propagation in these hearts.
• Remodeling of Gap Junctions in Mouse Hearts Hypertrophied by Forced Retinoic Acid Signaling: ?-MHC-hRAR? transgenic hearts show heterogeneous re-expression of (early) sarcomeric genes while expression of connexin43, N-cadherin and ?-catenin is down-regulated . We postulate that the resulting aberrant ventricular activation does not trigger development of lethal arrhythmias due to the small size of remaining healthy ventricular tissue where the transgene is not expressed.
• Gap Junction Remodeling in Hypertrophied Left Ventricles of Aortic-banded Rats: Prevention by Angiotensin II Type 1 Receptor Blockade*1: Electron microscopy of hypertrophied LV tissue revealed that Cx43-containin g gap junctions were frequently displaced from their usual locations to form side-to-side contacts distant from the disk, and also appeared as annular profiles. In aortic-banded rats treated with the angiotensin II (AII) type 1 receptor (AT1) antagonist, losartan (10 mg/kg/day, 11 weeks) not only LV hypertrophy, but also the gap junction disorganizatio n was markedly reduced. These results suggest that LV hypertrophy induced by pressure overload is associated with Cx43 gap junction disorganizatio n and that AII may play an important role either directly or indirectly in gap-junctional remodeling.

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