PROSTACYCLIN OVERPRODUCTION IN BARTTER'S SYNDROME

Hans Georg Güllner; FredericC Bartter; Chiara Cerletti; J. Bryan Smith; JohnR Gill

doi:10.1016/S0140-6736(79)92116-0

PROSTACYCLIN OVERPRODUCTION IN BARTTER'S SYNDROME

Hans Georg Güllner, FredericC Bartter, Chiara Cerletti, J. Bryan Smith, JohnR Gill

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Abstract

Urinary excretion of 6-keto-prostaglandin F₁α and thromboxane B₂, the major metabolites of prostacyclin and of thromboxane A₂, respectively, was measured by specific radioimmunoassays in five female patients with Bartter's syndrome and in five normal female controls. The patients with Bartter's syndrome excreted about four times as much 6-keto-PGF₁α as the controls; their excretion of thromboxane B₂ was no different from that of the controls. These data suggest that overproduction of prostacyclin mediates both the hyper-reninæmia and the hyporesponsiveness of blood-pressure to pressor agents in Bartter's syndrome.

Original language	English
Pages (from-to)	767-769
Number of pages	3
Journal	Lancet
Volume	314
Issue number	8146
DOIs	https://doi.org/10.1016/S0140-6736(79)92116-0
Publication status	Published - Oct 13 1979

ASJC Scopus subject areas

Medicine(all)

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title = "PROSTACYCLIN OVERPRODUCTION IN BARTTER'S SYNDROME",

abstract = "Urinary excretion of 6-keto-prostaglandin F1α and thromboxane B2, the major metabolites of prostacyclin and of thromboxane A2, respectively, was measured by specific radioimmunoassays in five female patients with Bartter's syndrome and in five normal female controls. The patients with Bartter's syndrome excreted about four times as much 6-keto-PGF1α as the controls; their excretion of thromboxane B2 was no different from that of the controls. These data suggest that overproduction of prostacyclin mediates both the hyper-renin{\ae}mia and the hyporesponsiveness of blood-pressure to pressor agents in Bartter's syndrome.",

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T1 - PROSTACYCLIN OVERPRODUCTION IN BARTTER'S SYNDROME

AU - Güllner, Hans Georg

AU - Bartter, FredericC

AU - Cerletti, Chiara

AU - Smith, J. Bryan

AU - Gill, JohnR

PY - 1979/10/13

Y1 - 1979/10/13

N2 - Urinary excretion of 6-keto-prostaglandin F1α and thromboxane B2, the major metabolites of prostacyclin and of thromboxane A2, respectively, was measured by specific radioimmunoassays in five female patients with Bartter's syndrome and in five normal female controls. The patients with Bartter's syndrome excreted about four times as much 6-keto-PGF1α as the controls; their excretion of thromboxane B2 was no different from that of the controls. These data suggest that overproduction of prostacyclin mediates both the hyper-reninæmia and the hyporesponsiveness of blood-pressure to pressor agents in Bartter's syndrome.

AB - Urinary excretion of 6-keto-prostaglandin F1α and thromboxane B2, the major metabolites of prostacyclin and of thromboxane A2, respectively, was measured by specific radioimmunoassays in five female patients with Bartter's syndrome and in five normal female controls. The patients with Bartter's syndrome excreted about four times as much 6-keto-PGF1α as the controls; their excretion of thromboxane B2 was no different from that of the controls. These data suggest that overproduction of prostacyclin mediates both the hyper-reninæmia and the hyporesponsiveness of blood-pressure to pressor agents in Bartter's syndrome.

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PROSTACYCLIN OVERPRODUCTION IN BARTTER'S SYNDROME

Abstract

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