Acetylcholine and potassium movements in rabbit auricles

Rayner, Barbara; Weatherall, M.

doi:10.1113/jphysiol.1959.sp006200

Cited by 56 publications

(28 citation statements)

References 21 publications

(31 reference statements)

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“…After immersion in radioactive medium the tissues were rinsed in 0 15M choline chloride, blotted, dried at 110°C for more than 2 hr, and were ashed and estimated for 42K and total K (Rayner & Weatherall, 1959).…”

Section: Methodsmentioning

confidence: 99%

“…The solutions were equilibrated throughout with 95% 02 + 5 % CO2. To minimize the risk of oxidation, the amines were added to the previously warmed and gassed ra'dioactive medium immediately before they were used experimentally.After immersion in radioactive medium the tissues were rinsed in 0 15M choline chloride, blotted, dried at 110°C for more than 2 hr, and were ashed and estimated for 42K and total K (Rayner & Weatherall, 1959).Potassium efflux was estimated at 290 C, but otherwise as described byRayner& Weatherall (1959). Auricles were placed in medium containing 42K immediately after dissection or 14 PHYSIO.…”

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confidence: 99%

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Adrenaline, noradrenaline and potassium fluxes in rabbit auricles

Waddell¹

1961

The Journal of Physiology

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The rate and force of rhythmic contraction in the heart are increased by adrenaline (Oliver & Schafer, 1895; Elliott, 1905) and noradrenaline (Ahlquist, 1948). Adrenaline increases the slope of the diastolic prepotential in pace-maker cells of spontaneously beating auricles (West, Falk & Cervoni, 1956), and both drugs increase the rate of repolarization after an action potential in all auricular cells (Brooks, Hoffman, Suckling & Orias, 1955). As repolarization after an action potential is generally assumed to be due to the passive efflux of potassium from the tissue, it would be expected that adrenaline and noradrenaline would accelerate this flux. There appears to be little published information about the effect of these amines on the resting membrane potential in quiescent left auricles, so it is difficult to predict what changes in potassium fluxes might be expected. The present paper describes observations on the potassium fluxes of left (quiescent) and right (spontaneously beating) rabbit auricles under the influence of noradrenaline and adrenaline, and enables a distinction to be made between effects on the fluxes through the resting membrane, and on fluxes in spontaneously contracting tissue. METHODSPotassium influx was measured over periods of 20 min as described by Rayner & Weatherall (1957), except that a temperature of 29°C was used instead of 370 C. Unstretched divided auricles were immersed for 1 hr in inactive saline medium, containing (mM): Na 145; K 5-8; Ca 1.7; Mg 1-2; Cl 128; HCO8 25; S04 1-2; H2P04 1.2; dextrose 11, and were then transferred to a similar medium containing some of the potassium as the isotope 42K and sometimes either noradrenaline bitartrate (4 x 10-5M) or adrenaline hydrochloride (4 x 10-5M) for 20 min. The solutions were equilibrated throughout with 95% 02 + 5 % CO2. To minimize the risk of oxidation, the amines were added to the previously warmed and gassed ra'dioactive medium immediately before they were used experimentally.After immersion in radioactive medium the tissues were rinsed in 0 15M choline chloride, blotted, dried at 110°C for more than 2 hr, and were ashed and estimated for 42K and total K (Rayner & Weatherall, 1959).Potassium efflux was estimated at 290 C, but otherwise as described byRayner& Weatherall (1959). Auricles were placed in medium containing 42K immediately after dissection or 14 PHYSIO. CLV

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Section: Methodsmentioning

confidence: 99%

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Adrenaline, noradrenaline and potassium fluxes in rabbit auricles

Waddell¹

1961

The Journal of Physiology

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“…Furthermore, a substantial increase in background current would not be expected on the basis of radioisotope (42K) data in mammalian atria. Rayner & Weatherall (1959) showed that even 2-0 x 10-M acetylcholine produced only very small (1.2-1-4 We acknowledge financial support from the M.R.C.…”

Section: Discussionmentioning

confidence: 99%

Changes in membrane currents in bullfrog atrium produced by acetylcholine.

Giles¹,

Noble²

1976

The Journal of Physiology

250

113

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SUMMARY1. A double sucrose-gap voltage-clamp technique has been used to study the effects of acetylcholine on the membrane currents in atrial trabeculae of the bullfrog, Rana catesbeiana.2. The second, or slow inward (Ca2+/Na+) current, was found to be markedly reduced by concentrations of acetylcholine greater than approximately 2-0 x 10-8 M. The resulting decrease in net calcium entry provides a straightforward explanation for the negative inotropic action of acetylcholine in atrial muscle.3. Measurements of membrane resistance near the resting potential showed that relatively high doses of acetylcholine (approximately 10-7 M) decrease membrane resistance by about twofold. This effect is shown to be the result of an increase in a time-independent background current which appears to be carried mainly by potassium ions.4. Using appropriate pharmacological techniques, it has been possible to demonstrate: (i) that the peak slow inward current is reduced to about half its initial value before any significant increase in background current occurs; (ii) that even when a sufficient dose of acetylcholine to produce an increase in background current is used, the background current shows inward-going rectification and cannot account for the observed reduction in the slow inward current.5. No consistent change was observed in the degree of activation of the time-dependent outward membrane currents after application of concentrations of acetylcholine which produced large decreases in the peak slow inward current.6. These results are discussed in relation to previous electro-physiological and radioisotope studies of the mechanism of the negative inotropic effect of acetylcholine in cardiac muscle.

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“…Then part of the K+ in each of the media was replaced with '2K+. The hearts were perfused with fluid containing '2K+ for 5, 10, 15 or 20 min, and then the "K+ and K+ contents of the atria and apices of the ventricles were determined as described by Rayner & Weatherall (1959).…”

Section: Methodsmentioning

confidence: 99%

Actions of adrenaline on the potassium balance of the isolated heart

Stafford

1969

British J Pharmacology

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1. The action of adrenaline on the K± balance of the isolated heart was found to depend on the ionic composition and the temperature of the perfusion fluids used. 2. When the perfusion fluid contained 145 mm Na+, 1.7 mM Ca++ and 3-9 mM K+, adrenaline caused the hearts to gain K+; when the K+ concentration was reduced to 1-2 mm, adrenaline caused a loss of K+. Both were actions on /3 receptors. 3. When the Ca++ or the Na+ concentration in the perfusion fluid was reduced, together with a reduction in K+, adrenaline no longer produced K+ loss from the hearts, but produced a gain of K+. 4. When the temperature of the perfusion fluid was reduced to 250 C, adrenaline still produced a gain of K+ by hearts perfused with fluid containing 3.2 mM K+, but did not produce a loss of K+ from hearts perfused with fluid containing 1.2 mm K+.Measurements of the action of adrenaline on K+ fluxes in isolated atria were made by Waddell (1961), and by Stafford (1962). Both authors were in agreement that the main action of adrenaline was to cause an increased uptake of K+ into the atria, thus producing a net increase in their K+ content. The action of adrenaline was studied mostly in concentrations ranging from 2 x 10-6M to 7.5 x 1O-5M, but higher concentrations produced the same effect. Melville, Mazurkiewicz & Korol (1955), however, found that adrenaline increased the rate of loss of K+ from isolated hearts perfused with K+-free fluid. Later, Melville & Korol (1958) showed that, in hearts perfused with several fluids containing different, K+ concentrations, adrenaline, noradrenaline or isoprenaline produced a net loss of K+ from the heart.Waddell ( 1961) and Stafford (1962), who found that adrenaline caused an increase in K+ content, were using atria and Melville and his co-workers, who found a decreased K+ content, were using isolated hearts, so it seemed possiible that the conflicting results could have been due to a difference between the actions of adrenaline on K+ fluxes in atrial and ventricular muscle; differences in the ionic composition of the fluid might also have been an important factor.

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Acetylcholine and potassium movements in rabbit auricles

Cited by 56 publications

References 21 publications

Adrenaline, noradrenaline and potassium fluxes in rabbit auricles

Adrenaline, noradrenaline and potassium fluxes in rabbit auricles

Changes in membrane currents in bullfrog atrium produced by acetylcholine.

Actions of adrenaline on the potassium balance of the isolated heart

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