Renal tubular transport of water, solute, and PAH in rats loaded with isotonic saline

Cortney, Marshall A.; Mylle, Margaret; Lassiter, William E.; Gottschalk, Carl W.

doi:10.1152/ajplegacy.1965.209.6.1199

Cited by 136 publications

(68 citation statements)

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“…In other studies in which whole kidney FF was compared with SNFF in normal rats (10,14), the former was measured by (19) found that less PAH appears in the final urine than is present in cortical distal tubules, a finding which we confirmed (10). This might mean that some PAH is reabsorbed in the collecting ducts.…”

Section: Filtration Fraction (Ff)supporting

confidence: 77%

A micropuncture study of renal salt and water retention in chronic bile duct obstruction.

Bank¹,

Aynedjian²

1975

J. Clin. Invest.

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Section: Filtration Fraction (Ff)supporting

confidence: 77%

A micropuncture study of renal salt and water retention in chronic bile duct obstruction.

Bank¹,

Aynedjian²

1975

J. Clin. Invest.

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“…Studies of TCH-o excretion in saline-loaded rats indicate that the sodium transport system in the ascending limb of the loop of Henle is unsaturable up to the highest rate of sodium delivery to the loop of Henle that can be-achieved in the intact animal (34). Cortney, Mylle, Lassiter, and Gottschalk (35) calculated from micropuncture studies that during hydropenia the proximal convolution of the rat nephron reabsorbed approximately three times as much sodium as the loop of Henle; the reabsorptive load per mass of tissue would therefore be roughly 8/3 as much in the loop as in the proximal convolution. During an infusion of isotonic saline, however, about 42% of the glomerular filtrate was reabsorbed in the proximal convolution and approximately the same amount in the loop.…”

Section: Methodsmentioning

confidence: 99%

The distribution of sodium-potassium-activated adenosine triphosphatase in medulla and cortex of the kidney

Hendler¹,

Torretti²,

Epstein³

1971

J. Clin. Invest.

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“…No INTRODUCTION It is now well established that the increase in urinary excretion of sodium which occurs during acute saline loading is due to a decrease in sodium reabsorption by the tubules rather than to an increase in the amount of sodium filtered by the glomeruli (1)(2)(3)(4)(5)(6)(7)(8). The mechanism (or mechanisms) responsible for this decrease in tubular reabsorption is not entirely clear.…”

mentioning

confidence: 99%

Effect of changes in renal perfusion pressure on the suppression of proximal tubular sodium reabsorption due to saline loading

Bank¹,

Koch²,

Aynedjian³

et al. 1969

J. Clin. Invest.

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AIB S T R A C T Rapid intravenous infusion of saline isknown to suppress reabsorption of sodium and water in the proximal tubule. It has previously been shown that this suppression is accompanied by two changes which in combination might account for the over-all decrease in reabsorption: a reduction in the intrinsic reabsorptive capacity of the tubular epithelium (C/rr') and a reduction in the ratio between tubular volume and GFR (7rrd/Vo). The present micropuncture experiments were carried out in order to study the possible role of altered peritubular physical forces (hydrostatic and colloid oncotic pressure) in mediating these two changes. Proximal tubular reabsorptive capacity, transit time, fractional reabsorption of sodium and water, 7rrd/Vo, and intratubular hydrostatic pressure were measured in salineloaded rats during acute changes in renal perfusion pressure induced by intermittent constriction of the abdominal aorta.We found that when renal perfusion pressure was lowered to 70-90 mm Hg, the usual effects of saline loading on C/irr, 7rrd/Vo, and fractional reabsorption in the proximal tubule were greatly minimized. When the aortic clamp was released and renal perfusion pressure allowed to rise, C/irr', 7rrd/Vo, and fractional reabsorption fell markedly to levels characteristically seen in saline diuresis. Reclamping of the aorta reversed all of these changes.In order to determine whether the changes in C/rr' accompanying changes in renal perfusion pressure were mediated by a circulating natriuretic hormone, we assayed in hydopenic rats the dialysate of plasma collected from saline-loaded rats during and after release of aortic constriction by the split oil drop method. No Dr. Norman Bank is a Career Scientist of the Health Research Council of New York City.Received for publication 21 June 1968 and in revised form 9 October 1968. significant difference in reabsorptive half-time (ti) was found between the two dialysates, and ti with both dialysates was approximately the same as was found when isotonic saline was injected in the tubules of hydropenic control animals. These observations suggest that the large changes in C/rr' which occurred with changes in renal perfusion pressure in saline-loaded rats were not mediated by a circulating hormone. We suggest that the reduction in C/ir', wr'd/Vo, and fractional reabsorption which occurs in the proximal tubule during a saline diuresis is related to the rise in hydrostatic pressure within the kidney. INTRODUCTIONIt is now well established that the increase in urinary excretion of sodium which occurs during acute saline loading is due to a decrease in sodium reabsorption by the tubules rather than to an increase in the amount of sodium filtered by the glomeruli (1-8). The mechanism (or mechanisms) responsible for this decrease in tubular reabsorption is not entirely clear. It has been shown by Rector, Sellman, Martinez-Maldonado, and Seldin (9) that acute saline loading in the rat is accompanied by two changes in the proximal tubule: a reduction in the intrins...

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Renal tubular transport of water, solute, and PAH in rats loaded with isotonic saline

Cited by 136 publications

References 0 publications

A micropuncture study of renal salt and water retention in chronic bile duct obstruction.

A micropuncture study of renal salt and water retention in chronic bile duct obstruction.

The distribution of sodium-potassium-activated adenosine triphosphatase in medulla and cortex of the kidney

Effect of changes in renal perfusion pressure on the suppression of proximal tubular sodium reabsorption due to saline loading

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