Direct stimulation of human erythrocyte membrane (Na+ + K+)-Mg ATPase activity invitro by physiological concentrations of d-aldosterone

Hamlyn, John M.; Duffy, Thomas J.

doi:10.1016/0006-291x(78)90191-2

Cited by 35 publications

(9 citation statements)

References 22 publications

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“…Other published in vitro studies showed that aldosterone stimulates Na + /К + -АТPase activity in human erythrocyte membranes (Hamlyn and Duffy, 1978). One possible explanation is that the incorporation leads to conformational changes and reorganization in the active center of the enzyme molecule of Na + /K + -ATPase.…”

Section: Thyroid and Steroid Hormonesmentioning

confidence: 95%

Protein Kinases and Protein Phosphatases as Participants in Signal Transduction of Erythrocytes

Maneva¹,

Maneva-Radicheva²

2012

Protein Kinases

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Section: Thyroid and Steroid Hormonesmentioning

confidence: 95%

Protein Kinases and Protein Phosphatases as Participants in Signal Transduction of Erythrocytes

Maneva¹,

Maneva-Radicheva²

2012

Protein Kinases

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“…On the other hand, reports are available indicating that mineralocorticoids can alter the Na + -K + pump and Na + permeability of human, rabbit, and dog erythrocytes, both in vivo and in vitro. 33 " 37 However, d-aldosterone (10-|2 -10" 6 M) did not affect ouabain-sensitive Li + uptake by human erythrocytes (Li + replacing external K + ) in vitro (Duhm J, unpublished results), indicating that the fourfold stimulation of Na + -K + ATPase by physiological concentrations of aldosterone reported for human erythrocyte ghosts 38 is not associated with a corresponding alteration of the transport function of the Na + -K + pump in intact human erythrocytes.…”

Section: Namentioning

confidence: 99%

Sodium and potassium ion transport accelerations in erythrocytes of DOC, DOC-salt, two-kidney, one clip, and spontaneously hypertensive rats. Role of hypokalemia and cell volume.

Duhm¹,

Göbel²,

Beck³

1983

Hypertension

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SUMMARY Sodium (Na + ) and potassium (K + ) transport by the furosemide-sensitive Na + -K + transport system, the Na + -K + pump, and the cation leak(s) were studied in erythrocytes from DOCwater, DOC-salt, two-kidney, one clip (Sprague-Dawley), and spontaneously hypertensive rats (Wistar-Kyoto). Rubidium (Rb + ) was used as a tracer for K + . After 4 weeks of DOC-salt hypertension, inward K + (Rb + ) transport by the furosemide-sensitive system was increased threefold, and the inward Na + leak and the red cell Na + content were elevated by about 50%. The rise in cell Na + accelerated K + inward and Na + outward transport by the Na + -K + pump. DOC-water hypertension caused similar but less pronounced changes. In two-kidney, one clip hypertension, the Na + leak and the Na + -K + pump rates were slightly elevated, and furosemide-sensitive Rb + uptake tended to be increased. In spontaneously hypertensive rats, furosemide-sensitive Rb

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“…More recently several investigators have demonstrated that aldosterone has a stimulatory effect on Na+,K+-ATPase activity in broken erythrocyte preparations and on cation fluxes in erythrocyte ghosts (Gall et al, 1971;Hamlyn & Duffy, 1978;Stem et al, 1983). We were unable to produce any stimulation of the enzyme in intact leucocytes in the short-term by measuring active cation fluxes, or Na+ ,K+-ATPase activity by Pi production on broken cell preparations.…”

Section: Carbenoxolonementioning

confidence: 99%

“…Cortisol also has mineralocorticoid properties, and can so act when present in high concentrations. Recent evidence has suggested that these adrenal steroids may regulate cellular ion transport in single human cells by a direct effect on Na+,K+-ATPase (Gall et al, 1971;Hamlyn & Duffy, 1978;Stern et al, 1983), though this area remains confused. The diterpenoid forskolin has recently been demonstrated to enhance renal cortex Na+ ,K+-ATPase activity, possibly through regulation by cAMP (Giesen et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

Action of compounds with effective in vivo mineralocorticoid activity on ion transport in leucocytes.

Baron¹,

Green²

1986

Brit J Clinical Pharma

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We have studied the in vitro short‐term effects of aldosterone (1.0‐ 1000 nmol l‐1), cortisol (0.5‐5.0 mumol l‐1), fludrocortisone (1.0‐10 nmol l‐1) and carbenoxolone (0.5‐3 mmol l‐1) on 86rubidium influx (a model for potassium), 22sodium efflux, and [3H]‐ouabain binding capacity in intact human leucocytes. No effect of aldosterone (at concentrations present in Conn's syndrome) or fludrocortisone could be demonstrated on cation fluxes or [3H]‐ouabain binding compared to controls. No significant effect of cortisol, at concentrations either physiological or present in Cushing's syndrome, could be demonstrated on cation fluxes or [3H]‐ouabain binding compared to controls. Carbenoxolone significantly increased 86Rb influx and 22Na efflux at concentrations known to cause hypokalaemia in man. The effect was not blocked by propranolol. No effect could be demonstrated for [3H]‐ ouabain binding.

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Direct stimulation of human erythrocyte membrane (Na+ + K+)-Mg ATPase activity invitro by physiological concentrations of d-aldosterone

Cited by 35 publications

References 22 publications

Protein Kinases and Protein Phosphatases as Participants in Signal Transduction of Erythrocytes

Protein Kinases and Protein Phosphatases as Participants in Signal Transduction of Erythrocytes

Sodium and potassium ion transport accelerations in erythrocytes of DOC, DOC-salt, two-kidney, one clip, and spontaneously hypertensive rats. Role of hypokalemia and cell volume.

Action of compounds with effective in vivo mineralocorticoid activity on ion transport in leucocytes.

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