“…Under these conditions in the present experiments, the facilitation also increased. This result suggests an accumulation of Ca rather than Na as the cause of facilitation because when the external Na is decreased, the inward Na current decreases (Brady & Woodbury, 1960). When the ratio of Ca/Na2 was constant and the concentration of Ca and Na varied, the initial tension response was the same (Luttgau & Niedergerke, 1958), and consistent with Niedergerke's (1963b) finding that the influx of Ca is constant under these conditions.…”
SUMMARY1. The magnitude and time course of the facilitation of contraction following previous stimulation have been studied in strips of frog ventricle when the external concentrations of Na and Ca were varied. The maximum tension and the maximum rate of rise of tension have been used as indices of activation of the contractile element. Under the experimental conditions these two parameters changed similarly.2. At low stimulus frequencies (3-12 beats/min), and moderate concentrations of external Ca (2-5 mM), the facilitation of contraction with repetitive stimulation can be predicted by assuming each contraction to produce an amount of facilitation which sums linearly with that remaining from previous responses. Thus, the staircase can be constructed from the decay of facilitation following a single contraction.3. The decay of facilitation appears to consist of two components. The first has a half-time of about 3 sec; the second about 50 sec. The decay of the second component of facilitation is slowed and its magnitude increased by raising the external Ca from 2 to 5 mm.4. Reducing the external Na concentration increases both the initial strength of contraction and the amount of facilitation.5. When the ratio Ca/Na2 is kept constant while changing the Ca and Na concentrations, the first contraction in a series remains constant, but facilitation is less at low concentrations of Ca and Na. Facilitation, therefore, does not depend solely on the amount of initial activation of the contractile system. 6. The results are consistent with the hypothesis that facilitation depends on the amount of calcium retained in some cellular store.
“…Under these conditions in the present experiments, the facilitation also increased. This result suggests an accumulation of Ca rather than Na as the cause of facilitation because when the external Na is decreased, the inward Na current decreases (Brady & Woodbury, 1960). When the ratio of Ca/Na2 was constant and the concentration of Ca and Na varied, the initial tension response was the same (Luttgau & Niedergerke, 1958), and consistent with Niedergerke's (1963b) finding that the influx of Ca is constant under these conditions.…”
SUMMARY1. The magnitude and time course of the facilitation of contraction following previous stimulation have been studied in strips of frog ventricle when the external concentrations of Na and Ca were varied. The maximum tension and the maximum rate of rise of tension have been used as indices of activation of the contractile element. Under the experimental conditions these two parameters changed similarly.2. At low stimulus frequencies (3-12 beats/min), and moderate concentrations of external Ca (2-5 mM), the facilitation of contraction with repetitive stimulation can be predicted by assuming each contraction to produce an amount of facilitation which sums linearly with that remaining from previous responses. Thus, the staircase can be constructed from the decay of facilitation following a single contraction.3. The decay of facilitation appears to consist of two components. The first has a half-time of about 3 sec; the second about 50 sec. The decay of the second component of facilitation is slowed and its magnitude increased by raising the external Ca from 2 to 5 mm.4. Reducing the external Na concentration increases both the initial strength of contraction and the amount of facilitation.5. When the ratio Ca/Na2 is kept constant while changing the Ca and Na concentrations, the first contraction in a series remains constant, but facilitation is less at low concentrations of Ca and Na. Facilitation, therefore, does not depend solely on the amount of initial activation of the contractile system. 6. The results are consistent with the hypothesis that facilitation depends on the amount of calcium retained in some cellular store.
“…However, this effect could not be the major cause, because the resting potential did not change significantly when excess chloride was replaced with nitrate and sulfate. The resting potential of 66 ±-2.6 my (mean 2 SE) in 170% Na Ringer's solution is very close to 67 4 2.6 mv (mean 4-2 SE) in NOs Ringer's solution and 66 4 2.6 (mean 4 2 sE) in SO 4 Ringer's solution. Moreover, to avoid this transient effect, the experiments were carried out 20 min after changing the soaking solutions.…”
Section: Relation Between [Na+] and The Maximum Rate Of Rise Of The mentioning
confidence: 56%
“…This value was remarkably lower than 560 -80 v/sec (mean 4 SE) for the Purkinje fiber of sheep (Weidmann, 1955) and one-third of 30 4-1.5 v/sec (mean -SE) for the frog ventricle (Brady and Woodbury, 1960 the action potential, defined here as duration measured at half-amplitude, was also prolonged with increase in external sodium concentration (Fig. 4).…”
Section: Relation Between [Na+] and The Maximum Rate Of Rise Of The mentioning
It already has been well documented that the maximum rate of depolarization and amplitude of action potentials are directly dependent on [Na+]o in the vertebrate myocardium. Almost all studies have been carried out at low sodium concentration ranges by substituting NaCl for other substances. Action potentials should be demonstrable in higher sodium concentrations, but cells are inevitably damaged by osmotic changes. The blood of elasmobranchs is nearly isosmotic with sea water, but NaCIl accounts for 54.5 % of the osmotic pressure and 38.7 % of it is maintained by urea molecules. Utilizing this special situation in elasmobranchs, the effect of high sodium concentration was studied up to 170 % of normal sodium concentration, while still retaining isosmotic condition. The rate of depolarization, amplitude, and duration of the myocardial action potential all increased in direct proportion to [Na 4 ],, and no depressant effect on transmembrane action potentials was observed in solutions of high sodium concentration. With regard to depolarization rate, the regression curve fitted by the least squares method passed through zero within two standard errors. At high sodium levels, the overshoot changed as expected theoretically, but at lower ranges it deviated from the theoretical values.[Na+] and [K+]i in this tissue have been determined, and these data are explained on the basis of the Na theory.
“…Under nembutal anesthesia (33 mg/kg) THE JOURNAL of CELL BIOLOGY • VOLUME 58, 1978 -pages [1][2][3][4][5][6][7][8][9][10] hearts were removed and immersed in a.bath containing tyrode solution at 37°C. The composition of the normal tyrode (in mmol/liter) was : NaCl 137 ; KCI 2 .7 ; CaC1 2 1 .8 ; MgCI 2 0 .5 ; tris-HCl buffer 5 .0 ; glucose 8.3 ; pH 6 .8-6.9 .…”
Section: Methodsmentioning
confidence: 99%
“…DISCUSSION An interesting feature of the effects of ionic lanthanum on the electrophysiological properties of Purkinje cells is the decrement in the rate of rise of the action potential upstroke . This action suggests that La+++ might interfere with the mechanisms of the inward sodium current necessary for the development of the upstroke of the electrical response (1,2,3,5,8) . This assumption is supported by the reports of Lettvin et al .…”
Section: Ultrastructural Localization Of Lanthanum Depositsmentioning
Perfusion of beating false tendons of the dog heart with ionic lanthanum produced drastic but reversible modifications of the excitability and the transmembrane action potential of Purkinje cells . Ultrastructural examination of these cells revealed the appearance of a fine extracellular precipitate detectable on unstained sections . In addition, specimens perfused with La+++ showed a striking increase in the contrast of the sarcolemma, particularly in gap junctions and in pinocytic vesicles . La+++ deposits were restricted to the cytoplasmic leaflets of the sarcolemma ; no precipitates were found at the plasma membrane of fibroblasts, endothelial and smooth muscle cells, or unmyelinated nerve fibers present in the same specimens . A selective deposition of La+++ was also observed in the sarcolemma of atrial and ventricular cells of dog, rabbit, and cat hearts, as well as in the membrane of the transverse tubular system of ventricular cells . Both the electrophysiological effects and the ultrastructural membrane deposits produced by La+++ disappeared when the specimens were subsequently perfused with phosphate-containing tyrode solution . These results tend to demonstrate that a distinctive feature of the sarcolemma of mammalian cardiac cells is the presence of regions with a high surface density of binding sites for polyvalent cations.
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