Factors affecting Potassium Balance During Frusemide Administration
- 1 August 1984
- journal article
- research article
- Published by Portland Press Ltd. in Clinical Science
- Vol. 67 (2) , 195-203
- https://doi.org/10.1042/cs0670195
Abstract
The effects of Na+ intake, the renin-angiotensin-aldosterone system and antidiuretic hormone (ADH) on K+ balance during 3 days of frusemide administration to 6 normal [human] subjects. Subjects received 40 mg of frusemide for 3 days during 3 different protocols: Na+ intake 270 mmol/day (high salt); Na+ intake 20 mmol/day to stimulate the renin-angiotensin-aldosterone system (low salt); Na+ intake 270 mmol/day plus captopril (25 mg/6 h) to prevent activation of the renin-angiotensin-aldosterone system. In a 4th protocol, a water load was given during high salt intake to prevent ADH release and then frusemide was given. During high salt intake, frusemide increased K+ excretion (UKV) over 3 h, but the loss was counterbalanced by subsequent renal K+ retention so that daily K+ balance was neutral. Durig low salt intake, the magnitude of the acute kaliuresis following the 1st dose of frusemide and the slope of the linear relationship between UKV and th log of frusemide excretion were increased compared with that found during the high salt intake. In addition, low salt intake abolished the compensatory renal retention of K+ after frusemide and cumulative K+ balance over 3 days of diuretic administration was uniformly negative (-86 .+-. 7 mmol/3 days; P < 0.001). Captopril abolished the rise in plasma aldosterone concentration induced by frusemide. The acute kaliuresis after frusemide was unchanged compared with that observed during high salt intake. The compensatory reduction in UKV occurring after the diuretic was slightly potentiated. In fact, captopril given without the diuretic induced a small positive K+ balance. When a water load was given concurrently with frusemide, the acute kaliuresis was > 30% lower compared with that seen with frusemide alone, even though the natriuretic response was unchanged. K+ balance is maintained when frusemide is given during liberal Na+ intake because acute K+ losses are offset by subsequent renal K+ retention; this compensatory K+ retention can be inhibited by aldosterone release which could account for the negative K+ balance seen during salt restriction; the short-term kaliuretic response to frusemide is augmented by release of both ADH and aldosterone whereas changes in K+ balance over 3 days of frusemide are dependent on plasma aldosterone concentration.This publication has 11 references indexed in Scilit:
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