Contractions induced by a calcium‐triggered release of calcium from the sarcoplasmic reticulum of single skinned cardiac cells.

Fabiato, A; Fabiato, F

doi:10.1113/jphysiol.1975.sp011026

Cited by 642 publications

(327 citation statements)

References 41 publications

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“…Recently, it has been reported for both skeletal (24)(25)(26) and cardiac muscles (27)(28)(29) that a small amount of calcium ion triggers a regenerative release of calcium ion which activates the contractile system. Thus, inhibition of such a calcium induced calcium-releasing mechanism may be involved in the inhibitory effect of diltiazem on the contractile force.…”

Section: Discussionmentioning

confidence: 99%

Electrical and Mechanical Responses to Diltiazem in Potassium Depolarized Myocardium of the Guinea Pig

Nakajima

Hoshiyama

Yamashita

et al. 1976

Japanese Journal of Pharmacology

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Abstract-Effectsof diltiazem on the electrical and mechanical activities of guinea pig papillary muscle were investigated in K-rich Tyrode's solution (KCI 12.7 mM). The electrical properties of cell membrane in K-rich solution were also examined in the ventricular muscle fibers. It was found that the overshoot as well as the maximum rate of rise (Vm1x) of the action potential were highly sensitive to the extracellular concentration of CaC12 in K-rich solution. Vmax was also affected by NaCI. Diltiazem at a lower concentration (1.1 x 10-' M) caused a reduction in the contractile force of K-depolarized papillary muscle without producing significant changes in the resting and action potentials. In the presence of a higher concentration of diltiazem (1.1 x 10-' M), the contractile force decreased concurrently with the change in the action potential. Addition of CaClz restored the original strength of contraction in parallel to the recovery of the action potential, especially in its overshoot and V~nax. From these results, it is inferred that diltiazem may decrease the contractile force of guinea pig papillary muscle either by interfering with the transmembrane calcium influx or by intracellularly reducing the free calcium ion concentration in the myoplasm.In previous experiments carried out in normal Tyrode's solution (KC1 2.7 mM) (1), it was shown that diltiazem (CRD-401), a new 1,5-benzothiazepine derivative (2) with a potent coronary vasodilating activity (3), has a property which interferes with the excitation contraction coupling in the isolated guinea pig myocardium. It was also suggested that the compound antagonizes calcium ion essential for muscle contraction, thus causing a reduction in the contractile force of the myocardium (1). On the other hand, it has been reported that the slow inward calcium or calcium-sodium current, as well as the fast inward sodium current, is involved in the generation of the action potential of cardiac muscle fibers under normal physiological conditions (4-13).The slow inward calcium current, which is assumed to play an important role in the excitation-contraction coupling in the cardiac muscle (8,12,(14)(15)(16)(17)(18)(19), is disclosed as a result of the inactivation of sodium carrying system when the extracellular concentration of KCI was increased (20)(21)(22)(23) muscle fibers in K-rich solution were also examined. MATERIALS AND METHODSIsolated papillary or ventricular muscle of the guinea pig was used. The experimental procedures were similar to those described in the previous papers (1, 13 Values were obtained 10 min after the concentration of KCI was increased from 2.7 to 12.7 mM. Each value is the mean l--SE of 20 experiments. R.P., resting potential; A.P., amplitude of the action potential; O.S., overshoot; V,,,,,x-, maximum rate of rise of the action potential; duration of A.P., duration of the action potential measured at 50 and 90°o repolarization. Significant difference (paired t-test); *P<0.01.mV (mean+SE of 20 experiments) 10 min after the increase in KCI conce...

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Section: Discussionmentioning

confidence: 99%

Electrical and Mechanical Responses to Diltiazem in Potassium Depolarized Myocardium of the Guinea Pig

Nakajima

Hoshiyama

Yamashita

et al. 1976

Japanese Journal of Pharmacology

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“…The subsequent application of ryanodine (1 /IM) strongly suppressed these ouabaininduced fast-type AAPs and abolished the automaticity (bottom trace). Thus, most of the fast-type automaticity is presumably mediated by the cyclic release of Ca from the SR. Caffeine in high concentrations (>_ 5 mM) seems to interfere with a function of the SR (FABIATO and FABIATO, 1975) and to increase the slow inward Cat + current ('Ca) (Sc1m EIDER and SPERELAKIS, 1975;YATANI et al, 1984). As can be seen in Fig.…”

Section: Resultsmentioning

confidence: 63%

Two differential mechanisms of automaticity in diseased human atrial fibers.

et al. 1988

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The ionic mechanisms of automaticity in spontaneously active preparations (n = 38) from "diseased" human atria were investigated. The cycle length (CL) of the automatic action potential (AAP) ranged from 0.6 to 4.5 s (mean + S.D.: 2.0 + 1.0 s). The AAP from preparations obtained from non-digitalized patients (group 1, n = 29) showed various CLs, in that 16 patients had a CL longer than 2.0 s (slow-type AAP) while in tissues from the other 13 patients, the CL was 2.0 s or less (fast-type AAP). On the other hand, all preparations obtained from the digitalized patients prior to cardiac surgery (group 2, n = 9) had the fast-type AAP (CL <_ 2.0 s). The slow-type AAP was accelerated and changed to the fast one after application of ouabain (1 µM) or by perfusing with 50% [Na + ]o Tyrode solution. Ryanodine (1 tiM), a specific inhibitor of calcium release from the sarcoplasmic reticulum (SR), markedly lengthened the CL of fast-type AAP, without affecting the slow-type AAP. In contrast, caffeine (15 mM) shortened the CL of the slow-type AAP and remarkably lengthened the CL of the fast-type AAP, as is the case in ryanodine. The rate of slow-type AAP was enhanced with an increase in [Ca2+]o and depressed with a decrease in [Ca2 +]o or with application of diltiazem, a Ca2 + channel blocker. The slow-type AAP was changed to the fast-type AAP by stretching the preparation by about 20%. In vitro preparations excised from patients with dilated atria revealed a shorter CL of AAPs. We conclude that in "diseased" human atrial preparations, the ionic mechanism responsible for generation of slow-and fast-type automaticity differs. Slow automaticity (CL >2.0 s) perhaps relates to activation of the slow inward Ca2 + current, while the fast-type automaticity (CL <2.0 s) is linked to cyclic increases in [Ca2 +]~.

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“…Sweitzer and Moss 1990;Linke et al 1993;Fukuda et al 1996;Fukuda and Ishiwata 1999;Sasaki et al 2005;2006). Notably, these oscillations are distinct from those observed in intact cardiac muscle, which are no longer observed following interference with the SR (Fabiato and Fabiato 1975a;Rieser et al 1979;Lappé and Lakatta 1980;Mulder et al 1989). In addition, SPOC is reportedly unaffected by addition of ryanodine (Linke et al 1993;Fukuda et al 1996).…”

Section: Spoc and The Auto-oscillatory Heartmentioning

confidence: 82%

SPontaneous Oscillatory Contraction (SPOC): auto-oscillations observed in striated muscle at partial activation

et al. 2011

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Contractions induced by a calcium‐triggered release of calcium from the sarcoplasmic reticulum of single skinned cardiac cells.

Abstract: Ca2+ to a critical level at which it released a fraction of the Ca2+ it contained. Each contraction was followed by a re-sequestration of Ca2+, the kinetics of which conditioned the duration of the cycles.6.

Cited by 642 publications

References 41 publications

Electrical and Mechanical Responses to Diltiazem in Potassium Depolarized Myocardium of the Guinea Pig

Electrical and Mechanical Responses to Diltiazem in Potassium Depolarized Myocardium of the Guinea Pig

Two differential mechanisms of automaticity in diseased human atrial fibers.

SPontaneous Oscillatory Contraction (SPOC): auto-oscillations observed in striated muscle at partial activation

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