Relaxing effects of catecholamines on mammalian heart

Morad, Martin; Rolett, Ellis L.

doi:10.1113/jphysiol.1972.sp009912

Cited by 192 publications

(55 citation statements)

References 32 publications

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“…Negative to -40 mV epinephrine enhanced the hyperpolarization-induced decrease in [Ca2+]i. These findings are consistent with the well-described tension-relaxant effect of epinephrine in cardiac muscle (29)(30)(31) and support the idea that the relaxant effect is independent of its tension potentiating effects.…”

supporting

confidence: 81%

Epinephrine enhances Ca2+ current-regulated Ca2+ release and Ca2+ reuptake in rat ventricular myocytes.

Callewaert

Cleemann

Morad

1988

Proc. Natl. Acad. Sci. U.S.A.

125

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The voltage dependence of the intracellular Ca2 + transients was measured in single rat ventricular myocytes with the fluorescent Ca24 indicator dye fura-2. The whole-cell voltage damp technique was used to measure the membrane current, and 0.9 mM fura-2 was loaded into the cell by including it in the dialyzing solution of the patch electrode. A mechanical light chopper operating at 1200 Hz was used to obtain simultaneous measurements of the intracellular Ca2+ activity with fluorescence excitation on either side of the isosbestic point (330 am and 410 nm). The symmetry of the two optical Ca24 signals was used as a criterion to guard against artifacts resulting, for instance, from motion. The voltage dependence of peak Ca2+ current and the Ca24 transient measured 25 ms after depolarizing clamps from a holding potential of -40 mV were bell-shaped and virtually identical. The Ca2+ entry estimated from the integral of the Ca2+ current (0 mV, 25 ms) corresponds to a 5-10 pM increase in the total intracellular Ca24 concentration, whereas the optical signal indicated a 100 FM increase in total intracellular Ca24. Repolarization of clamp pulses from highly positive potentials were accompanied by a second Ca2+ transient, the magnitude of which, when summed with that measured during depolarization, was nearly constant. Ryanodine (10 #M) had little or no effect on the peak Ca2+ current but reduced the magnitude of the early Ca2+ transients by 70-90%. Epinephrine (1 FM) increased the Ca2+ current and the Ca2+ transients, accelerated the rate of decline of the Ca2+ transients at potentials between -30 and + 70 mV, and reduced the intracellular [Ca2+] below baseline at potentials positive to + 80 or negative to -40 mV, where clamp pulses did not elicit any Ca2+ release. Elevation of intracellular cAMP mimicked the relaxant effect of epinephrine at depolarizing potentials, whereas elevation of extracellular [Ca2+] did not. These results suggest that most of the activator Ca2+ in rat ventricular cells is released from the sarcoplasmic reticulum as a graded response to sarcolemmal Ca2+ influx. Consistent with a graded Ca2+-induced Ca2+ release we find that epinephrine increases the internal Ca2+ release by increasing the Ca2+ current. Epinephrine may also increase the Ca2+ content of the sarcoplasmic reticulum that may, in turn,

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supporting

confidence: 81%

Epinephrine enhances Ca2+ current-regulated Ca2+ release and Ca2+ reuptake in rat ventricular myocytes.

Callewaert

Cleemann

Morad

1988

Proc. Natl. Acad. Sci. U.S.A.

125

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“…The responses of rat ventricular muscle in high-K solutions are similar to those reported by Gibbons & Fozzard (1971) and Morad & Rolett (1972). Increasing the tonicity induces significant contractures, and this effect may be responsible for the incomplete relaxation when KCl is added, although a direct interaction between depolarization and the osmotic effects cannot be excluded.…”

Section: Physiological Society November 1973supporting

confidence: 73%

Communications

1974

The Journal of Physiology

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In view of the controversy concerning the adequacy of nitrous oxide as an anaesthetic in cats (Russell, 1973; Blakemore et al. 1974) Base-line measurements were made using 80 % N20, 19% 02, 1 % CO2, which contains the highest concentration of N20 compatible with an adequate supply of oxygen. We gave repeated injections of procaine HCl around pressure points and wound margins to supplement the effect of the N20, and monitored the e.e.g. continuously. We also reintroduced halothane into the gas mixture at the first sign of lightening anaesthesia. The e.e.g. remained synchronized throughout the experiment.

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“…Boyett, Kirby & Orchard, 1988); it is conceivable, therefore, that the resulting changes in the action potential could abolish the lusitropic effect of isoprenaline. However, although ryanodine markedly reduces the size of the transient, this has little effect on the configuration of the action potential (White & Terrar, 1990) and, in any case, changes in the action potential appear to have little effect on the lusitropic effect of adrenergic stimulation, which persists during both shortening and lengthening of the action potential (Morad & Rolett, 1972), making it unlikely that changes in the action potential can explain the ryanodine-induced abolition of the lusitropic effect of isoprenaline.…”

Section: Discussionmentioning

confidence: 94%

The role of the sarcoplasmic reticulum in the response of isolated ferret cardiac muscle to beta‐adrenergic stimulation

Shah¹,

Than²,

White³

et al. 1994

Experimental Physiology

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SUMMARY,/-Adrenergic stimulation of cardiac muscle leads to an increase in the strength of contraction and an abbreviation of its time course. We have investigated the role of the sarcoplasmic reticulum in these changes by monitoring force and cytoplasmic [Ca2+] in ferret papillary muscles, and the Ca2+ current in isolated ferret myocytes, during the application of isoprenaline in the absence and presence of the sarcoplasmic reticulum inhibitor ryanodine (10-6 mol/l). Isoprenaline (10-6 mol/l) led to a marked increase in the size of both the twitch and Ca2+ transient, and a decrease in their duration. In the presence of ryanodine, application of isoprenaline had no significant effect on either the size or the time course of the twitch. However, the increase in the Ca2+ current in response to isoprenaline was the same in the absence and presence of ryanodine. Increasing bathing [Ca2+] led to a prolongation of both the twitch and the Ca2+ transient. In the presence of ryanodine, increasing bathing [Ca2+] still increased the size, but decreased the duration, of the twitch. These data provide direct evidence that both the inotropic and lusitropic effects of isoprenaline are mediated via the sarcoplasmic reticulum.

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Relaxing effects of catecholamines on mammalian heart

Cited by 192 publications

References 32 publications

Epinephrine enhances Ca2+ current-regulated Ca2+ release and Ca2+ reuptake in rat ventricular myocytes.

Epinephrine enhances Ca2+ current-regulated Ca2+ release and Ca2+ reuptake in rat ventricular myocytes.

Communications

The role of the sarcoplasmic reticulum in the response of isolated ferret cardiac muscle to beta‐adrenergic stimulation

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