The effect of chlorothiazide on renal excretion of electrolytes and free water

Heinemann, H.; Demartini, Felix E.; Laragh, John H.

doi:10.1016/0002-9343(59)90207-4

Cited by 121 publications

(56 citation statements)

References 13 publications

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“…Chlorothiazide has been shown to inhibit selectively sodium reabsorption at the cortical diluting segment [11]. The natriuretic effect of chlorothiazide in our patient was comparable to that seen in healthy subjects in whom the sodium load to the distal tubule was increased [8].…”

Section: Discussionsupporting

confidence: 66%

Studies on the Site of Renal Salt Loss in a Patient with Bartter's Syndrome

et al. 1973

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A child with growth retardation, hypokalemic alkalosis, and urinary salt losing is described. Pressor response to angiotensin II was reduced and renal biopsy showed striking hyperplasia of the juxtaglomerular apparatus.Renal tubular function was studied in the patient and in healthy control subjects during hypotonic saline diuresis. Glomerular filtration rate (GFR) was 128 ml/min/ 1.73 m 2 in the patient and 129 ±30 ml/min/1.73 m 2 in the control subjects. Fractional sodium delivery to the distal nephron, as estimated by (C H2 o + C Na )/100 ml GFR, was 13.3 ml and 11.1 ± 3.5 ml in the patient and normal subjects, respectively. Sodium transport at the diluting segment [(CH 2 O/CH 2 O + C Na ) X100] was markedly impaired in the patient, 32% versus 80% ± 9.2% in the control subjects. The natriuretic effect of chlorothiazide was normal in the patient, which suggests that the reabsorptive capacity of the thiazide-sensitive segment of the distal nephron is preserved. The evidence presented suggests that the defective reabsorption of sodium in the patient is due to an impaired sodium transport in the ascending limb of Henle's loop. The present study raises the possibility that a similar tubular defect may be responsible for the impaired renal handling of sodium that is often observed in patients with Bartter's syndrome. Speculation

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Section: Discussionsupporting

confidence: 66%

Studies on the Site of Renal Salt Loss in a Patient with Bartter's Syndrome

et al. 1973

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“…after the administration of meralluride in man (7,8). The prompt increase in free water clearance appears to be transient in nature and is associated with a modest solute diuresis.…”

Section: Discussionmentioning

confidence: 99%

“…Potassium secretion, however, which represents a late distal operation was shown to be depressed by the mercurial agents (5,6). In hydrated man, it was demonstrated that meralluride produced a prompt increase in the rate of excretion of "nonsolute obligated" water implying a proximal tubular effect on salt and water absorption (7,8). On the other hand, other observers reported that the administration of organomercurials to hydrated man and dog did not change the rate of free water clearance (9,10).…”

mentioning

confidence: 99%

Effect of Meralluride on Solute and Water Excretion in Hydrated Man: Comments on Site of Action*

Goldstein¹,

Levitt²,

Hauser³

et al. 1961

J. Clin. Invest.

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“…Metabolism ward techniques and the analytical methods for the measurement of plasma and urine electrolytes and blood urea nitrogen have been reported previously (17). None of the subjects had diarrhea during the studies and stool samples were not saved.…”

Section: Methodsmentioning

confidence: 98%

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

Brunner¹,

Baer²,

Sealey³

et al. 1970

J. Clin. Invest.

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223

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A B S T R A C T The effect of potassium administration and of dietary potassium deprivation on plasma renin activity and aldosterone excretion has been studied in 10 normal subjects and in 12 hypertensive patients maintained on a constant dietary regimen.Potassium administration reduced plasma renin activity in 18 of 28 studies of both normal and hypertensive subjects. Suppression of renin often occurred despite sodium diuresis induced by potassium administration. The renin suppression was related to induced changes in plasma potassium concentration and urinary potassium excretion.The failure of suppression of plasma renin in 10 studies could be accounted for by the smaller amounts of potassium administered to these subjects, together with a possibly overriding influence of an induced sodium diuresis.In six studies potassium deprivation invariably increased plasma renin activity even though a tendency for sodium retention often accompanied this procedure.The data indicate that both the suppression of plasma renin activity induced by potassium administration and the stimulation of renin activity which follows potassium depletion occur independently of associated changes in either aldosterone secretion or in sodium balance. However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance.These interactions between potassium and plasma renin could be mediated by an ill-defined extrarenal pathway. But the findings are more consistent with an

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The effect of chlorothiazide on renal excretion of electrolytes and free water

Cited by 121 publications

References 13 publications

Studies on the Site of Renal Salt Loss in a Patient with Bartter's Syndrome

Studies on the Site of Renal Salt Loss in a Patient with Bartter's Syndrome

Effect of Meralluride on Solute and Water Excretion in Hydrated Man: Comments on Site of Action*

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

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