PROSTACYCLIN OVERPRODUCTION IN BARTTER'S SYNDROME

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

Research output: Contribution to journalArticlepeer-review

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 languageEnglish
Pages (from-to)767-769
Number of pages3
JournalLancet
Volume314
Issue number8146
DOIs
Publication statusPublished - Oct 13 1979

ASJC Scopus subject areas

  • Medicine(all)

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