Action of thyroxine on active transport in isolated membranes of Bufo bufo

Green, K.; Matty, A. J.

doi:10.1016/0016-6480(63)90019-4

Cited by 34 publications

(9 citation statements)

References 19 publications

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“…This suggests that a certain minimal amount of thyroid hormone is necessary to maintain the maximum sodium reabsorptive capacity of the kidney. A direct effect of thyroxine on sodium transport has been demonstrated in the isolated toad bladder (27,28), and the present studies are compatible with a direct effect of thyroid hormone on the renal tubule. However, the data do not exclude an indirect action through some unknown or as yet unexplored mechanism, such as a natriuretic hormone (29) or a redistribution of renal blood flow (30,31 Concomitant with the failure for TCH20 to rise the absolute and fractional CNa were increasing more rapidly in the hypothyroid rats.…”

Section: Methodssupporting

confidence: 88%

Studies on the exaggerated natriuretic response to a saline infusion in the hypothyroid rat

Holmes¹,

Discala²

1970

J. Clin. Invest.

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A B S T R A C T The exaggerated natriuresis of hypothyroid rats receiving a 5% saline infusion was studied to determine the mechanism and the site within the nephron responsible for this increase in sodium excretion. Sodium clearance (CNa) and fractional sodium excretion were both demonstrated to be greater in hypothyroid rats for any amount of sodium infused. The rate of increase in fractional sodium excretion in response to saline loading was 3.4 times greater in hypothyroid animals. At the conclusion of the diuresis some of the hypothyroid animals excreted greater than 45% of the filtered sodium load, while no control animal excreted more than 12% of the filtered sodium load.The mean clearance of insulin during the saline diuresis was 36.6% lower (P < 0.001) in the hypothyroid rats. D-Aldosterone given to hypothyroid animals 3 hr before the experiment did not alter the magnitude or rate of increase in fractional sodium excretion. Inulin space determinations in nephrectomized rats revealed that extracellular fluid volume was contracted by 17.1% in the hypothyroid rats (P < 0.01). Plasma sodium was not significantly different in hypothyroid and control animals.A limit on solute free water reabsorption (T'Huo) per osmolar clearance (Co..) was demonstrated in the hypothyroid rats when these animals excreted greater than 12% of the filtered osmotic load. The limit on TCH20 formation was associated with an acceleration in the rate of sodium excretion and a decline in the rate of potassium excretion. Early in the diuresis when Co.., CNa, and TCH20 were comparable in hypothyroid and control Received for publication 5 January 1970.rats, the filtered sodium load was 31% lower (P < 0.01) in the hypothyroid animals. These findings indicate that diminished thyroid hormone activity decreases renal sodium reabsorptive capacity. Indirect evidence suggests that the distal and possibly the proximal tubules are the sites of this diminished sodium reabsorption in hypothyroid animals. INTRODUCTIONHypothyroidism has profound effects on salt and water metabolism in the rat. These are manifested by an increase in water consumption and excretion (1), inability to elaborate a maximally concentrated urine (2), exaggerated natriuresis during a water or saline diuresis (3,4), and impaired ability to conserve sodium, resulting in a negative sodium balance and death when sodium intake is restricted (5). Fregly, Cade, Waters, Straw, and Taylor (4,6) have demonstrated a decreased secretory rate and tubular response to aldosterone in hypothyroid rats, and they have proposed that thyroid insufficiency influences sodium reabsorption through this indirect mechanism. Reville and Stephan (7), however, have recently presented evidence in adrenalectomized hypothyroid rats which suggested that the alteration of sodium metabolism observed in hypothyroid animals was independent of adrenal function. In the present study several of the factors which regulate sodium reabsorption were evaluated with the hope of determining what mechanism might be responsi...

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Section: Methodssupporting

confidence: 88%

Studies on the exaggerated natriuretic response to a saline infusion in the hypothyroid rat

Holmes¹,

Discala²

1970

J. Clin. Invest.

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“…Alternatively, it can be postulated that an increase of sodium transport by the ascending limb of the loop of Henle, which is capable of keep ing up with the washout of the interstitium due to the osmotic diuresis (7) is responsible for the conservation of the concentrating capacity in our experimental conditions. The postulated increase of sodium transport by the ascending limb of the loop of Henle is consistent with the observations of M eldolesi (12), who reports that the administra tion of 3 :5 :3'-triiodo-L-thyronine to normal or thyroidectomized rats increases significantly the anaerobic glycolysis of the renal medulla; and also with the reported increase in sodium transport by the isolated toad bladder when thyroxine is added to the bathing fluid (6,11).…”

Section: Discussionsupporting

confidence: 79%

Urinary Concentrating Ability in Rats Treated with Thyroxine

Torretti¹,

Marusic²,

Martinez³

1968

Nephron

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The maximal antidiuretic response of thyroxine treated rats fed normal and low sodium diets was studied by analyzing urine volume, sodium, potassium, urea and total solute concentrations in urine, and plasma. Sodium, potassium, ammonia and urea were also measured in kidney cortex, medulla and papilla of rats fed a low sodium diet. The volume of urine collected, Cosm and T^CH₂O were significantly higher in treated than in control rats; whereas no significant difference could be demonstrated in the other parameters studied, except in V × U/P urea, which was significantly higher in thyroxine treated rats, suggesting an increase in GFR. These results support the hypothesis that the increased urine flow observed in thyroxine treated rats is the result of an osmotic diuresis. The conservation of the urinary concentrating ability in spite of the osmotic diuresis may be due either to the fact that the flow attained is not sufficiently high as to limit the urinary concentrating process, or because the concentrating mechanism of these rats is more efficient than that of the controls, a possibility which could be explained by the greater urea excretion of these animals or by an increase of the amount of sodium transported by the ascending limb of the loops of Henle.

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“…Thyroxine increases net sodium flux from the mucosal to the serosal surface of the toad bladder and skin [63], and enhances the permeability of these membranes to the passive movement o f chloride, urea, and water [96], Red cell Na content is increased [62] and J3K uptake decreased in hyperthyroid patients [7]. Similarly, thyroxine increases intracellular sodium and decreases intracellular potassium in the adult rat brain [136], an effect attributed to 'inhibition of the sodiumpotassium pump' [114], In contrast, Ismail-Beigi and E delm an reported in creased transmembrane Na and K concentration differences in liver, dia phragm and heart muscle [74] and increased oxygen consumption ofliver and kidney slices of rats treated with triiodothyronine [75], Both these effects were attributed to stimulation of transport Na-K-ATPase by the hormone.…”

Section: Sodium Potassium and Cell Membrane Functionmentioning

confidence: 99%

Thyroid Hormone and the Kidney

Katz

Emmanouel

Lindheimer

1975

Nephron

174

127

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Thyroid hormones affect both renal morphology and function. They are required for kidney growth and development, and thyroid deficiency results in decreased renal plasma flow and glomerular filtration rate and in impaired urinary concentration and dilution. Thyroid hormones also influence membrane transport and electrolyte metabolism, and alterations in mineral metabolism in hyperthyroidism frequently cause calcium nephropathy which affects renal function adversely. The kidney plays an important role in the peripheral metabolism of iodine and thyroid hormones, and thyroid function is altered in certain kidney diseases, particularly chronic renal failure. The pathogenesis of these alterations is currently under active investigation.

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Action of thyroxine on active transport in isolated membranes of Bufo bufo

Cited by 34 publications

References 19 publications

Studies on the exaggerated natriuretic response to a saline infusion in the hypothyroid rat

Studies on the exaggerated natriuretic response to a saline infusion in the hypothyroid rat

Urinary Concentrating Ability in Rats Treated with Thyroxine

Thyroid Hormone and the Kidney

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