Relation between intracellular sodium and twitch tension in sheep cardiac Purkinje strands exposed to cardiac glycosides.

Wasserstrom, J. Andrew; Schwartz, Daniel P.; Fozzard, Harry A.

doi:10.1161/01.res.52.6.697

Cited by 76 publications

(45 citation statements)

References 22 publications

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“…In sheep Purkinje fibres, Boyett et al (1986) observed hysteresis in the relation between twitch tension and aNa (measured with Na+-sensitive microelectrodes) on application and wash-off of strophanthidin; with 10-5 M-strophanthidin the maximum width of the hysteresis loop was I + 0-1 mm aNa (Levi & Boyett, 1991). The hysteresis had not been reported by previous authors working with sheep Purkinje fibres (Lee & Dagostino, 1982;Wasserstrom et al 1983) and has been discounted as an artifact associated with the Na+-sensitive microelectrode (Lee, 1985). In the present study we have observed a similar hysteresis in the relation between the twitch and aia in guinea-pig ventricular myocytes on application and wash-off of strophanthidin (Fig.…”

Section: Discussion Ana In Ventricular Myocytessupporting

confidence: 83%

“…Another factor contributing to the difference between ventricular myocytes and Purkinje fibres may be that there is greater scope for an increase in the strength of contraction in Purkinje fibres than in ventricular muscle. For example, the work of Eisner et al (1981Eisner et al ( , 1984 and Wasserstrom et al (1983) shows that in Purkinje fibres twitch tension can increase by up to 10 times during Na+-K+ pump inhibition. In contrast, in cat ventricular muscle (rate of stimulation, 0 67 Hz; 30°C; 1t12 mM-bathing Ca2+) an increase in the bathing Ca2+concentration to maximise twitch tension only increased twitch tension by 2 2 times (Allen, 1975).…”

Section: Intracellular Sodium Anvd Contractionmentioning

confidence: 99%

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The relationship between contraction and intracellular sodium in rat and guinea‐pig ventricular myocytes.

Harrison

McCall

Boyett

1992

The Journal of Physiology

101

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SUMMARY1. The contraction, measured optically, and the intracellular Na' activity (aNa), measured with the Na+-sensitive fluorescent dye SBFI, have been recorded simultaneously in rat and guinea-pig ventricular myocytes.2. In rat and guinea-pig ventricular myocytes at rest, a'a was 7 8 + 03 mM (n = 4) and 5-1 +0-3 mM (n = 16), respectively.3. When both rat and guinea-pig ventricular myocytes were stimulated at 1 Hz after a rest there was usually a gradual increase in twitch shortening (referred to as a 'staircase') over several minutes accompanied by an increase in a'a over a similar time course. Twitch shortening increased by 21+3 % (n = 6) and 20 + 4% (n = 16) (of steady-state twitch shortening during 1 Hz stimulation) per millimolar rise in aNa in rat and guinea-pig ventricular myocytes, respectively.4. When rat and guinea-pig ventricular myocytes were exposed to strophanthidin to block the Na+-K' pump, there were increases in twitch shortening and aia over similar time courses. Twitch shortening increased by 24 + 4 % (n = 5) and 20+3 % (n = 10) (of control twitch shortening) per millimolar rise in aNa in rat and guineapig ventricular myocytes respectively. 5. The inotropic effect of cardiac glycosides, such as strophanthidin, is widely regarded to be principally the result of the rise in aia. The similarity of the relation between twitch shortening and aia during the staircase and on application of strophanthidin suggests that the progressive increase in the strength of contraction during the staircase was also linked to the rise in aNa.6. In guinea-pig, but not rat, ventricular myocytes there was hysteresis in the relation between twitch shortening and a'a on application and wash-off of strophanthidin. This indicates that strophanthidin has another inotropic action in guinea-pig ventricular myocytes.7. A computer model of excitation-contraction coupling has been developed to simulate the staircase and the action of cardiac glycoside and to account for the relation between contraction and intracellular Na+.

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Section: Discussion Ana In Ventricular Myocytessupporting

confidence: 83%

Section: Intracellular Sodium Anvd Contractionmentioning

confidence: 99%

The relationship between contraction and intracellular sodium in rat and guinea‐pig ventricular myocytes.

Harrison

McCall

Boyett

1992

The Journal of Physiology

101

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“…Ouabain has been thought to increase the contraction through a Na+-Ca2+ exchange mechanism (Reuter & Seitz, 1968;Sheu & Fozzard, 1982;Wasserstrom et al, 1983;Eisner et al, 1984;Vassalle & Lee, 1984;Wier & Hess, 1984;Grupp et al, 1985). Ouabain inhibits Na'-K' ATPase and results in an accumulation of [NaJ]i.…”

Section: Discussionmentioning

confidence: 99%

Negative inotropic effects of disopyramide on guinea‐pig papillary muscles

Kondo

Mizukami

Shibata

1990

British J Pharmacology

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The inhibitory effects of disopyramide on electromechanical responses were investigated in guinea‐pig papillary muscles driven by electrical stimuli. Disopyramide up to 10−5 m did not cause a negative inotropic effect, while the maximum upstroke velocity of the action potential (dV/dtmax) was significantly decreased. At higher concentrations, this drug dose‐dependently inhibited the contraction, and dV/dtmax was further decreased. This inhibition of contraction was accompanied by a depression of the slow action potential in partially depolarized preparations by increasing [K+]o (26 mm). In preparations pretreated with nifedipine (10−6 m) and ryanodine (10−6 m), the contraction was almost completely inhibited. In such preparations, ouabain (2 × 10−6 m) markedly increased the contraction, probably through the Na+‐Ca2+ exchange mechanism. This contraction was inhibited by disopyramide above 10−8 m, and an almost complete inhibition was caused at 3 × 10−5 m. A similar inhibitory effect was observed on the contraction increased by the lowering of [Na+]o (36 mm). These results suggest that disopyramide at high concentrations inhibits Ca influx through slow Ca2+ channels and at low concentrations, it reduces the contraction increased through the Na+‐Ca2+ exchange mechanism. Disopyramide had a greater effect on cardiac contractility mediated by the Na+‐Ca2+ exchange mechanism.

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“…This effect correlates with an increase in intracellular Ca2+ Allen et al, 1984) and the development of a ' Author for correspondence. positive inotropic effect (Lee et al, 1980;Wasserstrom et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

“…Studies with ion-selective microelectrodes have provided convincing evidence that cardiac glycosides increase intracellular Na' activity in mammalian myocardium, probably by inhibition of active Na' extrusion from the cell via the ATP-driven Na' pump (Ellis, 1977;Deitmer & Ellis, 1978; Lee et al, 1980;Cohen et al, 1982;Daut, 1982;Wasserstrom et al, 1983). This effect correlates with an increase in intracellular Ca2+ Allen et al, 1984) and the development of a ' Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Potassium changes the relationship between receptor occupancy and the inotropic effect of cardiac glycosides in guinea‐pig myocardium

Bachmaier¹,

Ebner²,

Reiter³

1985

British J Pharmacology

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I K+ (2.4-15.6mmoll-') antagonized the positive inotropic effect of dihydro-ouabain. The concentration-effect curves became steeper with the shift to higher concentrations of the glycoside. At 1.2 mmol 1-Ca2+, an increase in K+ from 2.4 to 12 mmol 1-P' required tenfold higher concentrations of dihydro-ouabain to produce equal inotropic effects. This factor was reduced to four at 3.2 mmol I-, Ca2+ . The same change in K+ concentration, at 1.2 mmol 1-' Ca2+, diminished the inotropic effect of ouabain on rested-state contractions by a factor of six. 2 The positive inotropic effect of Ca2+ was also antagonized by K+ (1.2-12 mmol 1-'). Reduction of Na+ from 140 to 70 mmol 1-' abolished the antagonistic action of K+ (1.2-8.0 mmol 1-'). Moreover the inotropic effect of Ca2" was enhanced.3 Reduction of Na+, from 140 to 70 mmol -', antagonized the positive inotropic effect of dihydroouabain more at low (2.4 mmol l') than at high (8.0 mmol I') K+. Accordingly, the extent of the dihydro-ouabain-K+ antagonism was reduced. 4 When the K+ concentration was increased from 2.4 to 12mmoll-', [3H]-ouabain binding was reduced by a factor of three. This is less than the reduction in the inotropic effectiveness of ouabain or dihydro-ouabain. 5 Reduction of stimulation frequency from 1 to 0.1215 Hz did not significantly alter the antagonistic effect of K+. Diminution of Vmax of the action potential was observed only at K+ concentrations greater than 5.9 mmol 1-, whereas the resting membrane potential was continuously depolarized over the entire range of K+ concentrations. 6 The results support the view that the reduction in receptor affinity cannot be the sole cause of the antagonism between the glycoside and K+. Impairment of passive Na+ influx during diastole, due to the K+-dependent depolarization of the resting membrane potential, contributed to about one half of the glycoside-K+ antagonism.

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Relation between intracellular sodium and twitch tension in sheep cardiac Purkinje strands exposed to cardiac glycosides.

Cited by 76 publications

References 22 publications

The relationship between contraction and intracellular sodium in rat and guinea‐pig ventricular myocytes.

The relationship between contraction and intracellular sodium in rat and guinea‐pig ventricular myocytes.

Negative inotropic effects of disopyramide on guinea‐pig papillary muscles

Potassium changes the relationship between receptor occupancy and the inotropic effect of cardiac glycosides in guinea‐pig myocardium

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