The effect of acute diuretic treatment on peripheral aldosterone concentration or aldosterone secretion rate in the rat has not yet been reported. In the present experiments frusemide evoked a sixfold increase in mean peripheral aldosterone concentration within 2 h followed by a gradual fall lasting for at least 6h. Thus acute fluid depletion evoked hyperaldosteronism in the rat as effectively as in other species. The simultaneous increase of corticosterone values indicates a possible contribution of corticotrophin to this response albeit the mean corticosterone level was below 200 ng/ml. Pretreatment with indomethacin abolished the increase in peripheral aldosterone concentration 2 h after administration of frusemide. One hour later the effect of indomethacin was less pronounced, although a significant negative interaction (P<0.025) between frusemide and indomethacin was revealed even at this time by a four-sample modification of the d-test of Behrens & Fisher. No significant changes were observed in plasma Na+ or K+ levels. Both basal and frusemide-induced sodium and urine excretion rates were reduced by indomethacin; K+ excretion rate was unaffected.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism