Side-dependent effects of internal versus external Na and K on ouabain binding to reconstituted human red blood cell ghosts.

Bodemann, H. H.; Hoffman, Joseph F.

doi:10.1085/jgp.67.5.497

Cited by 72 publications

(47 citation statements)

References 45 publications

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“…In a recent study with red cell ghosts (Bodemann & Hoffman, 1976) Schwartz et al 1975). This particular structure of the region involved in the binding may occur once during each Na-K pump cycle.…”

Section: Resultsmentioning

confidence: 99%

Active Na—K transport and the rate of ouabain binding. The effect of insulin and other stimuli on skeletal muscle and adipocytes

Clausen¹,

Hansen²

1977

The Journal of Physiology

137

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SUMMARY1. The effect of stimulation or inhibition of active Na-K transport on [3H]ouabain binding has been investigated in isolated soleus muscles and adipocytes.2. In rat soleus muscle, the ouabain-sensitive component of 42K influx was stimulated by insulin (100 m-u/ml.), adrenaline (6 x 106 M), and by pre-incubation with veratrine (10-5 M) or in a K-free buffer. In all of these instances, the rate of ouabain binding was increased by 41-113%. Conversely, pre-treatment with tetracaine (0.2 mM) decreased the 42K-influx and diminished the rate of [3H]ouabain binding by 36 %.3. Neither insulin, adrenaline or tetracaine produced any detectable change in the total number of ouabain-binding sites (as measured under equilibrium conditions) in rat soleus muscle.4. In mouse and guinea-pig soleus muscle and in fat cells isolated from rats, insulin also increased the rate of [3H]ouabain binding without producing any significant change in the total number of ouabain-binding sites.5. Both in soleus muscle and the epididymal fat pad of the rat, there was a linear correlation between 42K influx and the initial rate of [3H]-ouabain binding.6. It is concluded that the rate of ouabain binding is determined significantly by the rate of active Na-K transport, but within the time intervals studied (4-6 hr) stimulation or inhibition of the Na pump does not lead to any appreciable change in the total number of Na pumps. It seems unlikely that the stimulation of active Na-K transport by insulin or adrenaline is due to unmasking or de novo synthesis of Na pumps.

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Section: Resultsmentioning

confidence: 99%

Active Na—K transport and the rate of ouabain binding. The effect of insulin and other stimuli on skeletal muscle and adipocytes

Clausen¹,

Hansen²

1977

The Journal of Physiology

137

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“…In red blood cells, for example, several studies indicate that K § competes with Na § for pump sites on the inside of the cell membrane, so that an increase in [K+]i decreases the amount of Na + pumped out of the cell (Garay & Garrahan, 1973;Knight & Welt, 1974;Simons, 1974;Bodemann & Hoffman, 1976;Blostein & Chu, 1977 …”

Section: Inactivation Of ~He Electrogenic Pumpmentioning

confidence: 99%

Effect of intracellular potassium upon the electrogenic pump of frog retinal pigment epithelium

1978

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We have studied the hyperpolarizing, electrogenic pump located on the apical membrane of the retinal pigment epithelium (RPE) in an vitro preparation of bullfrog RPE-choroid. Changes in RPE [K+]i alter the current produced by this pump. Increasing [K+]o in the solution perfusing the basal membrane increases RPE [K+]i (measured with a K+-specific microelectrode), and also depolarizes the apical membrane. The depolarization is due to a decrease in electrogenic pump current flowing across the apical membrane resistance, since it is abolished when the pump is inhibited by apical ouabain, by cooling the tissue, or by 0 mM [K+]o outside the apical membrane. Removal of Cl- from the solution perfusing the basal membrane abolishes the K+-evoked apical depolarization by preventing the entry of K+ (as KCl) into the cell. We conclude that the increase in [K+]i causes the decrease in pump current. This result is consistent with the finding that [K+]i is a competitive inhibitor of the Na+ - K+ pump in red blood cells. It is possible that the light-evoked changes in [K+]o in the distal retina could alter RPE [K+]i, and thus could affect the pump from both sides of the apical membrane. Any change in pump current is likely to influence retinal function, since this pump helps to determine the composition of the photoreceptor extracellular space.

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“…Evidence indicates that external K+ counteracts glycoside binding by inducing an allosteric configurational change of the transport system. Studies on reconstituted red cell ghosts (Bodemann and Hoffman, 1976a) have provided strong support for this concept. It could be shown that the binding of ouabain is not slowed by external K + if internal K + is replaced by isotonic concentrations of biologically inactive choline chloride.…”

Section: Interaction Of Cardiac Glycosides and Na+k+ Pumpmentioning

confidence: 93%

The current concept for the cardiac glycoside receptor

Bodemann

1981

Clinical Cardiology

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Summary: This brief review emphasizes the significance of the Na+,K+-ATPase or the Na+,K+ pump of the intact membrane as the pharmacological receptor for cardiac glycosides. The properties of this transport enzyme and the regulation of glycoside binding are described. An outline is given of the problems encountered and of the progress made in attempting to correlate the inotropic action of cardiac glycosides with the binding of these drugs to the heart muscle and with the inhibition of the Na+,K+ pump. Furthermore, the correlation of intracellular Ca 2+ activity and Na + concentration with the inhibition of the Na+,K+ pump is discussed. The existence of a digitalis-like endogenous activity may also indicate an important role of the Na+,K+ pump as a receptor for a physiological regulatory control of cardiac contractility.

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Side-dependent effects of internal versus external Na and K on ouabain binding to reconstituted human red blood cell ghosts.

Cited by 72 publications

References 45 publications

Active Na—K transport and the rate of ouabain binding. The effect of insulin and other stimuli on skeletal muscle and adipocytes

Active Na—K transport and the rate of ouabain binding. The effect of insulin and other stimuli on skeletal muscle and adipocytes

Effect of intracellular potassium upon the electrogenic pump of frog retinal pigment epithelium

The current concept for the cardiac glycoside receptor

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