Effect of Sodium Restriction and Angiotensin II Infusion in Bartter's Syndrome

Sann, L; Dávid, M; Richard, Ph.; Floret, D.; Sassard, J; Bizollon, C; François, R

doi:10.1203/00006450-197612000-00005

Cited by 4 publications

(2 citation statements)

References 16 publications

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“…In favor of such a hypothesis is the failure of infused angiotensin, a known potent inhibitor of renin secretion [10] to lower plasma renin in most [22. 52,91] although not all [83] studies. The original objection to this proposal lack of autonomy of renin secretion to such known modulators as postural change, volume ex pansion.…”

Section: Juxtaglomerular Hyperplasiamentioning

confidence: 99%

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Bartter’s Syndrome – A Dilemma of Cause and Effect

Bourke

Delaney

1981

Nephron

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Six interrelated abnormalities of Bartter’s syndrome are analyzed – juxtaglomerular hyperplasia, angiotensin resistance, altered kallikrein-kinin system, hyperprostaglandinuria, hypokalemia, and chloride-losing nephropathy. Arguments are advanced that any one of these could be the proximate cause and result in all the others. By the same token, each abnormality could be a consequence of any of the others and, furthermore, modulate the others by negative or positive feedback. Despite many recent insights, available data do not permit a definitive conclusion as to the locus of the primary abnormality. Rather, the syndrome presents as a remarkable biological counterpart to an electronic integrated circuit. The altered physiology of Bartter’s syndrome is reviewed and the pathogenesis of the syndrome analyzed in the light of recent literature.

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Section: Juxtaglomerular Hyperplasiamentioning

confidence: 99%

“…Al though originally assumed to be entirely explicable on the basis of secondary aldosteronism ( fig. I), neither aminoglutethamide, an inhibitor of aldosterone biosynthesis [44,83], nor bilateral adrenalectomy [95.96], permanently correct the hypokalemia.…”

Section: Juxtaglomerular Hyperplasiamentioning

confidence: 99%