Effects of adrenalectomy and hormone replacement on Na- K-ATPase in renal tissue

Ed, Hendler; Torretti, Jorge; Lr, Kupor; Fh, Epstein

doi:10.1152/ajplegacy.1972.222.3.754

Cited by 83 publications

(36 citation statements)

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“…Discrepancy between our results and those reported (1,2) concerning the time course of change in Na,K-ATPase activity may be explained by any one of the following factors: 1) the rats used in our ex periments were non-adrenalectomized.…”

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confidence: 91%

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EFFECT OF ALDOSTERONE ON RENAL Na,K-ACTIVATED ADENOSINE-TRIPHOSPHATASE ACTIVITY IN NON-ADRENALECTOMIZED RATS

Ikeda

Inagaki

et al. 1979

Japanese Journal of Pharmacology

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It has been reported that the activity of Na, K-activated adenosinetriphosphatase (Na,K-ATPase) in the kidney is reduced by adrenalectomy and that the activity is restored by administration of aldosterone (1, 2). However, with the adrenalectomized rats, the restoration of the enzyme by aldosterone has been shown to take much longer time (i.e. 6-24 hr) as compared with the time (1-2 hr) for the maximal effect of aldosterone on the sodium reabsorption (3). We attempted to determine whether or not aldosterone stimulates Na,K-ATPase in correlation with the enhancement of Na reabsorption in non-adrenalec tomized rats.Male Wistar rats weighing 170-250 g were used. Each animal was given water (3 ml p.o.) and pitressin tannate in oil (0.5 U i.m), and then anesthetized 1 hr later with pen tobarbital sodium (30 mg/kg i.p.). Administration of 5 % mannitol through the femoral vein was started at a rate of 0.1 ml/ruin and continued during the experiment. After a 30 min equilibration period, one 30-min urine collection was made and then aldosterone (10 /tg per animal) was given i.v. to animals of the experimental group. The control animals were infused with 5 % mannitol through the experiment. The bladder was catheterized and sodium and potassium in the urine were determined by flame photometry (Hitachi 205), and the chloride content by a chloridemeter (Hiranuma, Chloride Counter CL-3). To determine the activities of Mg and Na,K-ATPase, animals were sacrificed and the kidney

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contrasting

confidence: 91%

“…It has been reported that the activity of Na, K-activated adenosinetriphosphatase (Na,K-ATPase) in the kidney is reduced by adrenalectomy and that the activity is restored by administration of aldosterone (1,2). However, with the adrenalectomized rats, the restoration of the enzyme by aldosterone has been shown to take much longer time (i.e.…”

mentioning

confidence: 99%

EFFECT OF ALDOSTERONE ON RENAL Na,K-ACTIVATED ADENOSINE-TRIPHOSPHATASE ACTIVITY IN NON-ADRENALECTOMIZED RATS

Ikeda

Inagaki

et al. 1979

Japanese Journal of Pharmacology

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“…One possible explanation is that the hormone does not act directly on Na+/K+ ATPase, but rather facilitates entry of Na+ ions into the cell, which in turn would stimulate the Na+ pump. In support of this possibility, Sharp & Leaf (1966) have suggested that in the kidney, where corticosterone also stimulates ATPase activity (Chignell & Titus, 1966;Hendler, Torretti, Kupor & Epstein, 1972), the Na+-retaining property ofthe corticosteroids is due to synthesis of a specific permease enzyme which increases membrane permeability to Na+.…”

Section: Discussionmentioning

confidence: 99%

THE POSSIBLE INVOLVEMENT OF Na+ IONS IN CORTICOSTERONE‐INDUCED HYPERCONTRACTILITY IN THE RAT ANOCOCCYGEUS MUSCLE

Gibson

Pollock

1976

British J Pharmacology

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The possibility that corticosterone‐induced hypercontractility in the rat anococcygeus muscle might be due to an intramuscular redistribution of Na+ was investigated. The contractility of the isolated muscle to noradrenaline (NA) was directly dependent on the Na+ concentration of the Krebs solution. There was a linear relationship between the maximum contractile response of the muscle to NA and the Na+ concentration of the Krebs solution. Muscle contractility was also increased by the presence of ouabain (10−4m) in the bathing medium. Muscles from rats treated with corticosterone exhibited increases in both total and ouabain‐sensitive ATPase activity. The relationship between corticosterone, Na+ distribution, and muscle contractility is discussed.

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“…Two types of compound relevant to this effect, adrenocortical steroids and diterpenoids, have known actions on ion flux through different mechanisms involving Na+, K+-ATPase. Aldosterone is the main sodium retaining hormone and regulator of extracellular fluid volume, mainly through the action it exerts on the sodium 'pump' via receptors in the distal portion of the nephron (Jorgensen, 1969;Hendler et al, 1972;Charney et al, 1974). Cortisol also has mineralocorticoid properties, and can so act when present in high concentrations.…”

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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Effects of adrenalectomy and hormone replacement on Na- K-ATPase in renal tissue

Cited by 83 publications

References 0 publications

EFFECT OF ALDOSTERONE ON RENAL Na,K-ACTIVATED ADENOSINE-TRIPHOSPHATASE ACTIVITY IN NON-ADRENALECTOMIZED RATS

EFFECT OF ALDOSTERONE ON RENAL Na,K-ACTIVATED ADENOSINE-TRIPHOSPHATASE ACTIVITY IN NON-ADRENALECTOMIZED RATS

THE POSSIBLE INVOLVEMENT OF Na+ IONS IN CORTICOSTERONE‐INDUCED HYPERCONTRACTILITY IN THE RAT ANOCOCCYGEUS MUSCLE

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

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