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 | |
| Publication status | Published - Oct 13 1979 |
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ASJC Scopus subject areas
- Medicine(all)
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PROSTACYCLIN OVERPRODUCTION IN BARTTER'S SYNDROME. / Güllner, Hans Georg; Bartter, FredericC; Cerletti, Chiara; Smith, J. Bryan; Gill, JohnR.
In: Lancet, Vol. 314, No. 8146, 13.10.1979, p. 767-769.Research output: Contribution to journal › Article
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TY - JOUR
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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U2 - 10.1016/S0140-6736(79)92116-0
DO - 10.1016/S0140-6736(79)92116-0
M3 - Article
VL - 314
SP - 767
EP - 769
JO - The Lancet
JF - The Lancet
SN - 0140-6736
IS - 8146
ER -