The Role of Chloride in Hypokalemic Alkalosis in the Rat*

Struyvenberg, A; Graeff, J. De; Lameijer, L. D. F.

doi:10.1172/jci105146

Cited by 22 publications

(9 citation statements)

References 18 publications

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“…6 In addition there is an experimental study which does not prove intracellular acidosis in hypokalemic alkalosis7 These reports appear to be compatible with the results of our present study.…”

Section: Discussionsupporting

confidence: 92%

Urinary Citrate Excretion in Primary Aldosteronism

Shioji

Rikimaru

Ito

1967

Tohoku J. Exp. Med.

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Section: Discussionsupporting

confidence: 92%

Urinary Citrate Excretion in Primary Aldosteronism

Shioji

Rikimaru

Ito

1967

Tohoku J. Exp. Med.

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“…7). Selective repletion with K or Cl only partially repaired the alkalosis and GFR, while KCl repaired both, as has been previously described (13,30,33,42). The rat is more "chloride-resistant" than dog or man with respect to repair of alkalosis with NaCl (13,29,30).…”

Section: Resultsmentioning

confidence: 55%

“…That isolated dietary K depletion, as in groups IVB and IVc, can sustain metabolic alkalosis has long been known for the rat (5,29,30) and for man (31,32), though not for the dog. Mineralocorticoid treatment (e.g., DOCA), as in group IIIA, is also a well established cause of persisting metabolic alkalosis associated with K deficiency (13,29,33), simulating primary hyperaldosteronism.…”

Section: Resultsmentioning

confidence: 99%

“…In the following analysis, an attempt is made to illustrate the empiric relationship of changes in GFR that were evoked by alterations in K and/or Cl stores. For this purpose, alteration in K stores is reflected by changes in muscle [K] (30), and alteration in Cl stores is reflected according to its impact on renal hemodynamics by changes in plasma volume (8,9). The effect of changes in K and Cl stores on changes in GFR can be expressed quantitatively using multiple linear regression analysis.…”

Section: Resultsmentioning

confidence: 99%

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Metabolic alkalosis in the rat. Evidence that reduced glomerular filtration rather than enhanced tubular bicarbonate reabsorption is responsible for maintaining the alkalotic state.

Cogan¹,

Liu²

1983

J. Clin. Invest.

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A B S T R A C T Maintenance of chronic metabolic alkalosis might occur by a reduction in glomerular filtration rate (GFR) without increased bicarbonate reabsorption or, alternatively, by augmentation of bicarbonate reabsorption with a normal GFR. To differentiate these possibilities, free-flow micropuncture was performed in alkalotic Munich-Wistar rats with a glomerular ultrafiltrate total CO2 concentration of 46.5±0.9 mM (vs. 27.7±0.9 mM in controls). Alkalotic animals had a markedly reduced single nephron GFR compared with controls (27.4±1.5 vs. 51.6±1.6 nl/min) and consequently unchanged filtered load of bicarbonate. Absolute proximal bicarbonate reabsorption in alkalotic animals was similar to controls (981±49 vs. 1,081±57 pmol/min), despite a higher luminal bicarbonate concentration, contracted extracellular volume, and potassium depletion. When single nephron GFR during alkalosis was increased toward normal by isohydric volume expansion or in another group by isotonic bicarbonate loading, absolute proximal bicarbonate reabsorption was not substantially augmented and bicarbonaturia developed. To confirm that a fall in GFR occurs during metabolic alkalosis, additional clearance studies were performed. Awake rats were studied before and after induction of metabolic alkalosis associated with varying amounts of potassium Portions of this work were presented at the National Meet-

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“…During the experimental induction of potassium depletion in rats these coexistent factors are often present [9], but the typical vacuoles of proximal tubules described in clinical cases are never seen. This discrepancy in morpho logical findings may be attributed to a species difference.…”

Section: Introductionmentioning

confidence: 99%

A Correlated Study of Kidney Function and Ultrastructure in Potassium-Depleted Rats

Sarkar¹,

Levine²

1975

Nephron

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In order to provide an ultrastructural description of kaliopenic nephropathy in rats, potassium deficiency uncomplicated by chloride depletion or extracellular fluid volume expansion was induced by dietary means alone. After 12 days, serum and muscle analyses demonstrated severe potassium depletion, while urine concentrating ability was markedly impaired. Although micropuncture techniques demonstrated that net fluid transport in proximal tubules was normal, the epithelial cells showed the following morphological alterations: electron-lucent vacuoles and lysosome-like dense bodies were numerous, focal cytoplasmic degradation was present, and intercellular spaces were dilated in many proximal tubules. Medullary cell droplets were characterized by fusion, massive enlargement with sequestration of cytoplasmic components such as ribosomes, and occasional extrusion through ruptured plasma membranes – features not previously reported.

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The Role of Chloride in Hypokalemic Alkalosis in the Rat*

Cited by 22 publications

References 18 publications

Urinary Citrate Excretion in Primary Aldosteronism

Urinary Citrate Excretion in Primary Aldosteronism

Metabolic alkalosis in the rat. Evidence that reduced glomerular filtration rather than enhanced tubular bicarbonate reabsorption is responsible for maintaining the alkalotic state.

A Correlated Study of Kidney Function and Ultrastructure in Potassium-Depleted Rats

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