Evidence for a prostaglandin-independent defect in chloride reabsorption in the loop of henle as a proximal cause of Bartter's syndrome

Gill, John R.; Bartter, Frederic C.

doi:10.1016/0002-9343(78)90794-5

Cited by 219 publications

(130 citation statements)

References 29 publications

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“…In addition, these findings may provide a link between increased chloride reabsorption in the early distal tubule in salt-sensitive hypertension and blood pressure elevation (Kirchner, 1990;Roman & Kaldunski, 1991) and, conversely, between the defect in chloride reabsorption in the loop of Henle and the hypotension in Bartter's syndrome (Gill & Bartter, 1978). This effect of chloride on vasoactivity may explain the requirement for chloride as the anion accompanying sodium in salt-sensitive (Boegehold & Kotchen, 1989) and AII-dependent (Passmore & Jimenez, 1991;Sato et al, 1991) models of hypertension.…”

Section: Discussionmentioning

confidence: 99%

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Quilley

Lin

McGiff

1993

British J Pharmacology

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Section: Discussionmentioning

confidence: 99%

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Quilley

Lin

McGiff

1993

British J Pharmacology

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“…Chloride reabsorption was determined according to the method of Gill and Bartter [8] Her growth curve is shown in Fig. 1.…”

Section: Methodsmentioning

confidence: 99%

“…The cause is unknown but slightly increasing blood pressure after this age may be related. Gill et al [8] suggested that defective chloride reabsorption may be a primary cause of Bartter's syndrome and reported that indomethacin did not improve the defect in chloride reabsorption.…”

Section: Methodsmentioning

confidence: 99%

Long-Term Follow-Up of a Girl with the Neonatal Form of Bartter's Syndrome.

et al. 1997

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Abstract.We followed up a girl with the neonatal form of Bartter's syndrome for sixteen years and determined the sensitivity to angiotensin II before and during the indomethacin treatment.A 4-monthold girl was admitted to our hospital, because of severe hypokalemia and growth retardation. Initially we treated her with spironolactone and potassium supplements. This treatment increased plasma potassium levels and her growth. At the age of one year she was diagnosed as having Bartter's syndrome.Since then she has been treated with indomethacin at an initial dose of 3 mg/kg/day combined with spironolactone and potassium. After the start of the indomethacin treatment, her growth increased dramatically, and her final height was normal adult height. Her puberty developed normally and menarche occurred at the age of 12 years. Levels of serum sodium, chloride, plasma aldosterone and urinary prostaglandin E2 were also normalized. Levels of angiotensin I and II were improved but not within the normal range, but plasma potassium levels slightly decreased after plasma aldosterone levels were normalized and did not change during the treatment period. Plasma renin activity remained high until about the age of 8 years, after which it decreased to almost within the normal range. At 5 months after the start of indomethacin (3 mg/kg/day), her vascular sensitivity to angiotensin II had been improved, and after 2 years and 5 months, her vascular sensitivity was further improved. At this time renin activity had decreased after angiotensin II infusion, but plasma aldosterone did not change. At the age of 16 years (dose of indomethacin: 0.5 mg/kg/day), plasma aldosterone increased after angiotensin II infusion. These data suggest that indomethacin and spironolactone are effective treatments for the neonatal form of Bartter's syndrome, especially during childhood.

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“…An identity between these transport systems may also be deduced from the known inability of patients with myotonia congenita to concentrate their urine as effectively as normals (Campion & Peter, 1974). Therefore myotonia congenita could well be the result of a generalised disorder of chloride transport having some affinities with Bartter's syndrome, where the defect is postulated to be one of chloride reabsorption in the thick ascending limb of the loop of Henle (Gill & Bartter, 1978). Weakness, cramps, tetany and an inability to concentrate urine are typical features of Bartter's syndrome (Bartter, Pronove, Gill & MacCardle, 1962).…”

Section: Discussionmentioning

confidence: 99%

Myotonia as a Side Effect of Diuretic Action

Bretag

Dawe

Kerr

et al. 1980

British J Pharmacology

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1 Commonly used loop diuretics produce side effects in man which are similar to chemically induced myotonia. These diuretics have structural affinity with known myotonic agents. 2 We have observed EMG myotonia in vivo in leg muscles of rats treated with intravenous frusemide. 3 In the presence of several different diuretics, rat isolated diaphragm, soleus and extensor digitorum longus muscles as well as frog sartorius muscles produce typically myotonic contractions with relaxation times up to several seconds. 4 Intracellular recording of action potentials from diuretic-treated muscles reveals long lasting after-discharges following a brief electrical stimulus, again typical of chemically induced myotonia. 5Having demonstrated a myotonic action of several diuretics we suggest a need for caution in using these drugs in persons with hereditary myotonia and a need to be aware of possible provocation of myotonia in subclinical cases. Myopathies and neuropathies which are known to result from chronic exposure to myotonic agents also need to be considered. 6 In our study, the diuretic, acetazolamide, unmasked subthreshold myotonia. This seems to be at variance with reports of its usefulness in the treatment of myotonia. 7 Diuretics should probably not be employed in the treatment of herbicide intoxication where their myotonic activity would be expected to add to the known myotonic activity of the herbicide.

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Evidence for a prostaglandin-independent defect in chloride reabsorption in the loop of henle as a proximal cause of Bartter's syndrome

Cited by 219 publications

References 29 publications

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Long-Term Follow-Up of a Girl with the Neonatal Form of Bartter's Syndrome.

Myotonia as a Side Effect of Diuretic Action

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