Action potential duration and force-frequency relationship in isolated rabbit, guinea pig and rat cardiac muscle

1996 ◽  
Vol 166 (2) ◽  
pp. 150-155 ◽  
Author(s):  
P. Szigligeti ◽  
C. Pankucsi ◽  
T. B�ny�sz ◽  
A. Varr� ◽  
P. P. N�n�si
1986 ◽  
Vol 251 (6) ◽  
pp. H1106-H1110 ◽  
Author(s):  
P. Stemmer ◽  
T. Akera

Increases in stimulation frequency between 0.3 and 2 Hz decrease developed tension in rat, seemingly inconsistent with the explanation that an elevation of intracellular Na+-ion concentration is responsible for the positive force-frequency relationships observed in most species. Thus the force-frequency relationships were reevaluated in isolated atrial muscle of rat and mouse heart that show negative relationships, comparing them with ferret and guinea pig that show positive relationships. Ryanodine (2 nM, 45-min exposure) markedly reduced potentiated postrest contractions in all four species and caused a marked negative inotropic effect especially at low stimulation frequencies in rat and mouse, a moderate effect in ferret, but only a modest effect in guinea pig. In the presence of ryanodine, all four species showed positive force-frequency relationships. These results indicate that activator calcium in rat, mouse, and ferret cardiac muscle has a large ryanodine-sensitive component that shows a negative force-frequency relationship, masking a component for positive force-frequency relationships that exists in all species.


2007 ◽  
Vol 293 (1) ◽  
pp. H563-H573 ◽  
Author(s):  
Julio Altamirano ◽  
Donald M. Bers

Ca2+ current ( ICa) recovery from inactivation is necessary for normal cardiac excitation-contraction coupling. In normal hearts, increased stimulation frequency increases force, but in heart failure (HF) this force-frequency relationship (FFR) is often flattened or reversed. Although reduced sarcoplasmic reticulum Ca2+-ATPase function may be involved, decreased ICa availability may also contribute. Longer action potential duration (APD), slower intracellular Ca2+ concentration ([Ca2+]i) decline, and higher diastolic [Ca2+]i in HF could all slow ICa recovery from inactivation, thereby decreasing ICa availability. We measured the effect of different diastolic [Ca2+]i on ICa inactivation and recovery from inactivation in rabbit cardiac myocytes. Both ICa and Ba2+ current ( IBa) were measured. ICa decay was accelerated only at high diastolic [Ca2+]i (600 nM). IBa inactivation was slower but insensitive to [Ca2+]i. Membrane potential dependence of ICa or IBa availability was not affected by [Ca2+]i <600 nM. Recovery from inactivation was slowed by both depolarization and high [Ca2+]i. We also used perforated patch with action potential (AP)-clamp and normal Ca2+ transients, using various APDs as conditioning pulses for different frequencies (and to simulate HF APD). Recovery of ICa following longer APD was increasingly incomplete, decreasing ICa availability. Trains of long APs caused a larger ICa decrease than short APD at the same frequency. This effect on ICa availability was exacerbated by slowing twitch [Ca2+]i decline by ∼50%. We conclude that long APD and slower [Ca2+]i decline lead to cumulative inactivation limiting ICa at high heart rates and might contribute to the negative FFR in HF, independent of altered Ca2+ channel properties.


1995 ◽  
Vol 268 (6) ◽  
pp. H2321-H2328 ◽  
Author(s):  
S. Zhang ◽  
T. Sawanobori ◽  
H. Adaniya ◽  
Y. Hirano ◽  
M. Hiraoka

Effects of extracellular magnesium (Mg2+) on action potential duration (APD) and underlying membrane currents in guinea pig ventricular myocytes were studied by using the whole cell patch-clamp method. Increasing external Mg2+ concentration [Mg2+]o) from 0.5 to 3 mM produced a prolongation of APD at 90% repolarization (APD90), whereas 5 and 10 mM Mg2+ shortened it. [Mg2+]o, at 3 mM or higher, suppressed the delayed outward K+ current and the inward rectifier K+ current. Increases in [Mg2+]o depressed the peak amplitude and delayed the decay time course of the Ca2+ current (ICa), the latter effect is probably due to the decrease in Ca(2+)-induced inactivation. Thus 3 mM Mg2+ suppressed the peak ICa but increased the late ICa amplitude at the end of a 200-ms depolarization pulse, whereas 10 mM Mg2+ suppressed both components. Application of 10 mM Mg2+ shifted the voltage-dependent activation and inactivation by approximately 10 mV to more positive voltage due to screening the membrane surface charges. Application of manganese (1-5 mM) also caused dual effects on APD90, similar to those of Mg2+, and suppressed the peak ICa with slowed decay. These results suggest that the dual effects of Mg2+ on APD in guinea pig ventricular myocytes can be, at least in part, explained by its action on ICa with slowed decay time course in addition to suppressive effects on K+ currents.


1959 ◽  
Vol 197 (6) ◽  
pp. 1199-1204 ◽  
Author(s):  
Brian F. Hoffman ◽  
John J. Kelly

The unusual relationship between frequency of contraction and tension developed by the isolated rat papillary muscle has been studied in detail. The progressive decrease in tension with increasing rate is unrelated to the size or weight of the muscle and is not changed by alterations in the ionic composition of the perfusion medium. The force-frequency relationship is also unchanged by addition of plasma, epinephrine or digitalis to the perfusion medium. Rat papillary muscle is similar to other preparations of cardiac muscle with respect to recovery of contractility and the development of rest contractions and postextrasystolic potentiation.


1983 ◽  
Vol 245 (1) ◽  
pp. H7-H16 ◽  
Author(s):  
S. L. Lipsius

The influence of electrotonic interactions on propagation within the SA node was studied by recording transmembrane potentials simultaneously from two neighboring (less than 1 mm apart) subsidiary pacemaker cells within the sinoatrial (SA) node of the guinea pig. As single premature stimuli were delivered progressively earlier in diastole, retrograde propagation between cells was delayed progressively. Cells activated earlier displayed secondary depolarizations that were coincident with the depolarization of neighboring cells activated later. The secondary depolarizations increased action potential duration markedly. Rapid pacing elicited secondary depolarizations that resulted in a progressive increase in action potential duration and decrease in upstroke amplitude. These changes were associated with a progressive delay in retrograde propagation that led to intermittent block with Wenckebach periodicity. Exposure to tetrodotoxin (10(-5) g/ml) delayed antegrade propagation, resulting in electrotonically mediated secondary depolarizations and exit block with Wenckebach periodicity. It is concluded that delayed activation and electrotonically mediated interactions between cells can increase action potential duration and refractoriness. These changes contribute to progressive delays in propagation that may result in intermittent block with Wenckebach periodicity within the SA node.


1989 ◽  
Vol 67 (7) ◽  
pp. 734-739
Author(s):  
Hideharu Hayashi ◽  
Hajime Terada ◽  
Alexander Kholopov ◽  
Terence F. McDonald

The action potential configuration, developed tension, and resting tension were monitored in normoxic and hypoxic guinea pig papillary muscles superfused with solutions containing no substrate, glucose, or acetate (1–10 mM). In normoxic muscle, acetate provoked a concentration-dependent transient depression of the action potential duration and force of contraction, depression was maximal after 10–30 min, and recovery was complete after 90–120 min. In hypoxic muscle, acetate accelerated functional rundown (action potential shortening, decline of developed tension, increase in resting tension). Because rundown in hypoxic muscle was sensitive to factors affecting glycolysis (moderated by external glucose; accentuated by 2-deoxyglucose), the accentuated rundown with acetate may be accounted for by a partial block of glycolysis. However, block of glycolysis cannot explain the acetate-induced transient depression in normoxic muscle, since the depression was enhanced in normoxic muscle with 2-deoxyglucose-blocked glycolysis. We suggest that the transient depression is due to a transient depression of high energy nucleotides with consequent effects on ionic currents.Key words: acetate, action potential duration, 2-deoxyglucose, hypoxia, ATP.


Sign in / Sign up

Export Citation Format

Share Document