?-Adrenergic modulation of transient inward current in guinea-pig cardiac myocytes

1989 ◽  
Vol 415 (3) ◽  
pp. 276-288 ◽  
Author(s):  
M. Boller ◽  
L. Pott
Keyword(s):  
Guinea Pig ◽  
Cardiac Myocytes ◽  
Inward Current ◽  
Transient Inward Current ◽  
Adrenergic Modulation

Caffeine-induced Ca2+ release activates Ca2+ extrusion via Na+-Ca2+ exchanger in cardiac myocytes

1989 ◽  
Vol 257 (1) ◽  
pp. C147-C152 ◽  
Author(s):  
G. Callewaert ◽  
L. Cleemann ◽  
M. Morad
Keyword(s):  
Guinea Pig ◽  
Cardiac Myocytes ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Whole Cell ◽  
Inward Current ◽  
Fura 2 ◽  
Transient Inward Current ◽  
Inward Currents

Rapid application of caffeine in fura-2-dialyzed and whole cell-clamped rat and guinea pig ventricular myocytes activated reversibly large intracellular Ca2+ transients that accompanied Na+-dependent transient inward currents. Such transient inward currents had the same time course as the intracellular Ca2+ transient and were suppressed by Ni2+ and removal of extracellular Na+. Because Ca2+ release signals were not altered by addition of Ni2+ or removal of Na+, we concluded that the rise in intracellular Ca2+ concentration was necessary for the activation of the transient inward current. Thus the caffeine-induced transient inward current represents efflux of Ca2+ via the Na+-Ca2+ exchanger.

Effects of R-56865 on transient inward current, Na+-Ca2+ exchange, and Ca2+ release from SR in cardiac myocytes

1994 ◽  
Vol 267 (1) ◽  
pp. 1-1
Author(s):  
H. Ichikawa ◽  
D. J. Hearse ◽  
W. A. Coetzee
Keyword(s):  
Cardiac Myocytes ◽  
Inward Current ◽  
Transient Inward Current ◽  
R 56865

Pages H511–H520: H. Ichikawa, D. J. Hearse, and W. A. Coetzee. “Effects of R-56865 on transient inward current, Na+-Ca2+ exchange, and Ca2+ release from SR in cardiac myocytes.” The concentration of R-56865 should be 1 μM and not 1 mM as stated in the paper.

Effects of acidosis on Na+/Ca2+ exchange and consequences for relaxation in guinea pig cardiac myocytes

1994 ◽  
Vol 267 (2) ◽  
pp. H477-H487 ◽  
Author(s):  
C. M. Terracciano ◽  
K. T. MacLeod
Keyword(s):  
Guinea Pig ◽  
Cardiac Myocytes ◽  
Intracellular Acidosis ◽  
Rapid Cooling ◽  
Inward Current ◽  
Fluorescence Transient ◽  
Isolated Cardiac Myocytes ◽  
Rate Of Decline ◽  
The Times ◽  
Exchange Activity

We investigated the effect of intracellular acidosis (imposed by NH4Cl prepulses) on the relaxation and decline in intracellular Ca2+ (using indo 1 fluorescence) of isolated cardiac myocytes from the guinea pig. Acidosis produced a decrease in contraction and a prolongation of the fluorescence transient. The rate of decline in fluorescence after a rapid-cooling contracture was slower in acidosis compared with control. The decline in fluorescence after a rapid-cooling contracture in the presence of 10 mM caffeine was greatly slowed during acidosis, suggesting that Na+/Ca2+ exchange is affected. We recorded indo 1 fluorescence and the transient inward current in voltage-clamped cells on rapid application of 10 mM caffeine under control conditions and in acidosis. The amplitude of the transient increase in fluorescence was reduced in acidosis and the decline in fluorescence slowed. The current showed no difference in amplitude in acidosis, but the time to 50% recovery was increased by 57%. When amiloride or ethylisopropylamiloride was present, no differences in the current were found between control and acidosis, and the times to 50% recovery were similar. We conclude that intracellular acidosis slows Ca2+ efflux via Na+/Ca2+ exchange because of an increase in intracellular Na+ due to enhanced Na+/H+ exchange activity.

Modulation of action potential by [Ca2+]i in modeled rat atrial and guinea pig ventricular myocytes

2002 ◽  
Vol 282 (3) ◽  
pp. H1047-H1054 ◽  
Author(s):  
Chunlei Han ◽  
Pasi Tavi ◽  
Matti Weckström
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Action Potential ◽  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Transient Increase ◽  
Current Increase ◽  
Inward Current ◽  
Gp Model ◽  
Long Action

We simulated mechanisms that increase Ca2+ transients with two models: the Luo-Rudy II model for guinea pig (GP) ventricle (GP model) representing long action potential (AP) myocytes and the rat atrial (RA) model exemplifying myocytes with short APs. The interventions were activation of stretch-gated cationic channels, increase of intracellular Na+ concentration ([Na+]i), simulated β-adrenoceptor stimulation, and Ca2+accumulation into the sarcoplasmic reticulum (SR). In the RA model, interventions caused an increase of AP duration. In the GP model, AP duration decreased except in the simulated β-stimulation where it lengthened APs as in the RA model. We conclude that the changes in the APs are significantly contributed by the increase of the Ca2+ transient itself. The AP duration is controlled differently in cardiac myocytes with short and long AP durations. With short APs, an increase of the Ca2+ transient promotes an inward current via Na+/Ca2+-exchanger lengthening the AP. This effect is similar regardless of the mechanism causing the increase of the Ca2+ transient. With long APs the Ca2+ transient increase decreases the AP duration via inactivation of the L-type Ca2+ current. However, L-type current increase (as with β-stimulation) increases the AP duration despite the simultaneous Ca2+ transient augmentation. The results explain the dispersion of AP changes in myocytes with short and long APs during interventions increasing the Ca2+transients.

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