Membrane current changes in left ventricular myocytes isolated from guinea pigs after abdominal aortic coarctation

Ryder, Kathryn; Bryant, Simon M.; Hart, George

doi:10.1093/cvr/27.7.1278

Cited by 88 publications

(72 citation statements)

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“…The experiments conducted in this study were designed to limit the activation of 'K by using short voltage clamp pulses to 0 mV; other workers have reported that the activation of IK in guinea-pig ventricular myocytes under similar conditions is limited (Matsuura et al 1987;Ryder et al 1993). However, the results of Fig.…”

Section: The Delayed Rectifier Ikmentioning

confidence: 96%

The role of the Na(+)‐Ca2+ exchanger in the rate‐dependent increase in contraction in guinea‐pig ventricular myocytes.

Harrison

Boyett

1995

The Journal of Physiology

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1. The intracellular sodium activity (aN^), contraction and membrane current were recorded simultaneously in voltage-clamped guinea-pig ventricular myocytes. 2. Increasing the frequency (from 0 5 to 3 Hz) of voltage clamp pulses to 0 mV from a holding potential of -80 mV led to an increase in both a'a and contraction. The ratedependent increase in contraction was reduced by 25 ,UM tetrodotoxin (TTX) and abolished with a holding potential of -40 mV. There was no rate-dependent rise in a'Na with a holding potential of -40 mV. These results suggest an important role for a' a and in particular Na+ influx via Na+ channels during rate-dependent changes in contraction. 3. After an increase in frequency from 0'5 to 3 Hz, membrane current at the end of voltage clamp pulses became progressively more outward and the tail current upon repolarization became progressively more inward compared with those recorded at 0 5 Hz. ITTX reduced the magnitude of both the outward and inward rate-dependent shifts of current. 4. The addition of extracellular CsCl blocked the inward rectifier potassium current (IK 1) and the delayed rectifier (IK), but did not change the rate-dependent shift in current. 5. The difference between current-voltage relationships at 0 5 and 3 Hz showed that the rate-dependent outward shift of current at the end of voltage clamp pulses was small at potentials negative to -20 mV, was larger at more positive potentials and was reduced by TTX at most potentials. The TTX-sensitive component reversed at -47 mV.6. These results are consistent with a net increase in outward Na+-Ca2+ exchange current during a voltage clamp pulse in response to the rise of aia. The increase in outward current (resulting from either enhanced Ca2+ influx or reduced Ca2+ efflux) will augment the Ca2+ load of the cell and contribute to the rate-dependent increase in contraction.

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Section: The Delayed Rectifier Ikmentioning

confidence: 96%

The role of the Na(+)‐Ca2+ exchanger in the rate‐dependent increase in contraction in guinea‐pig ventricular myocytes.

Harrison

Boyett

1995

The Journal of Physiology

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“…Previous studies on left ventricular trabeculae (Meszaros & Levai, 1990, 1992Meszaros, 1992) (Kleiman & Houser, 1988;Scamps et al 1990;Bouron, Potreau & Raymond, 1992;Cerbai, Barbieri, Li & Mugelli, 1994) although in mild (Ryder et al 1993) and moderate (Keung, 1989) hypertrophy, an increase in ICa density has been reported. Only in severe cardiac hypertrophy, in which congestion is present, has ICa density been reported to decrease (Nuss & Houser, 1991; Rossner, 1991;Aiba & Creazzo, 1992;Hatem, Sham & Morad, 1994; LeGrand, Hatem, Deroubaix, Couetil & Coraboeuf, 1994;Ming, Nordin, Sirn & Aronson, 1994).…”

Section: Discussionmentioning

confidence: 83%

“…Single left ventricular myocytes from the rat hearts were obtained according to the method described previously (Ryder, Bryant & Hart, 1993). The cells were stored at room temperature in Dulbecco's modified Eagle's medium with 2 mg/ml Ultraser G (Gibco BRL, Paisley, UK) for up to 8 h.…”

Section: Cell Isolationmentioning

confidence: 99%

L‐type calcium current in catecholamine‐induced cardiac hypertrophy in the rat

Meszaros

Coutinho²,

Bryant³

et al. 1997

Experimental Physiology

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SUMMARYThis study investigates whether an increase in L-type calcium current (Ica) could explain the prolongation of the action potential associated with the cardiac hypertrophy produced by repeated administration of isoprenaline. Hypertrophy was induced by daily injection of isoprenaline (5 mg/kg i.p.) for 7 days in male Wistar rats. Under whole-cell voltage-clamp conditions, ICa was evoked in Na+-and Kt-free solution, by step depolarizations from a holding potential of -45 mV in single left ventricular myocytes isolated from control and hypertrophied rat hearts. In the test group, heart weight to body weight ratio and cell membrane capacitance were increased by 30 and 34%, respectively. Peak 'Ca was increased by 26 % (control, -1 46 + 0.06 nA, n = 17; hypertrophy, -1 85 + 0.13 nA, n = 19; P < 0.02). However, when normalized for cell capacitance, there was no significant difference in peak current density (control, -12 1 + 0-5 pA/pF; hypertrophy, -11-5 + 0 6 pA/pF). The voltage dependence of ICa was similar in both cell types. No change was observed either in the steady-state activation or inactivation kinetics, or in the time course of inactivation. The recovery from inactivation of ICa' when fitted with a monoexponential function with time constant Trec was not changed significantly by hypertrophy (control, Tree = 115 + 23 ms, n = 9; hypertrophy, Trec = 120 + 12 ms, n = 15). The increased calcium current occurs in parallel with the increase in cell size. The prolonged action potential duration seen in this model must be explained by changes in currents other than L-type calcium current.

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“…In right ventricular hypertrophy, Ica density has been reported to decrease by some investigators, 1,5) or be unchanged by others. 9) In left ventricular hypertrophy, Ica density has been reported to decrease, 5) increase, 3,4) or be unchanged. 7,8) Lee, et al 11) has raised a possible comprehensive interpretation of these controversial results, suggesting that the Ica density varied according to the stage of the acquired hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

“…1,2) In contrast to the Ito density, the results for the changes in inward L-type calcium current (Ica) in hypertrophic hearts remain controversial. Some have reported an increase in its density, 3,4) but others a decrease. 1,5,6) Moreover, no changes in its density have been noted.…”

mentioning

confidence: 99%

Time- and Subunit-dependent Differential mRNA Expression of L-type Ca2+ Channel during Progression of Right Ventricular Hypertrophy.

et al. 2001

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SUMMARYTo clarify the molecular basis for changes in L-type calcium channel (VLCC) density in ventricular hypertrophy, we analyzed the mRNA expression of all the subunits including the main subunit α1c and auxiliary subunits (α2δ, β2 and β3) composing VLCC in rat right ventricular hypertrophy (RVH) induced by monocrotaline injection. To test the hypothesis that the expression of each subunit might change differently during progression of RVH, leading to an altered electrophysiologic outcome for VLCC, we investigated the ratio of the mRNA level of each auxiliary subunit to the main subunit. After monocrotaline injection, α1c mRNA showed a transient decrease on the 14th day and thereafter significantly increased to reach approximately 1.8 fold that of the control level on the 21st day. The auxiliary subunit α2δ mRNA showed a pattern similar to that of α1c.The β3 mRNA increased rapidly after monocrotaline injection and increased approximately 4.1 fold. On the other hand, β2 mRNA showed no significant changes. Accordingly, only the mRNA ratio of β3 to α1c showed a significant increase among the auxiliary subunits after the monocrotaline injection. The ratio increased to a maximum of approximately 5.7 fold on the 14th day and thereafter decreased. These results suggest that VLCC density may be modified not only by α1c but also by its auxiliary subunit expression in ventricular hypertrophy, and provide a clue for understanding the controversial electrophysiologic results on VLCC density in hypertrophied hearts. (Jpn Heart J 2001; 42: 617-625)

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Membrane current changes in left ventricular myocytes isolated from guinea pigs after abdominal aortic coarctation

Cited by 88 publications

References 0 publications

The role of the Na(+)‐Ca2+ exchanger in the rate‐dependent increase in contraction in guinea‐pig ventricular myocytes.

The role of the Na(+)‐Ca2+ exchanger in the rate‐dependent increase in contraction in guinea‐pig ventricular myocytes.

L‐type calcium current in catecholamine‐induced cardiac hypertrophy in the rat

Time- and Subunit-dependent Differential mRNA Expression of L-type Ca2+ Channel during Progression of Right Ventricular Hypertrophy.

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