In an animal model, the vascular response to bumetanide, including increased renal blood flow, appears to be mediated by kinins and can be inhibited by indomethacin.
Bumetanide renal effects in animals should not guide clinical practice; leaves open kinin mediation for mechanistic studies.
Bumetanide (0.25 mg/kg intravenously) increases kidney volume by 20% at maximal diuresis in anaesthetized dogs. The kidney expansion is initially accompanied by a 2-4 fold increase in the subcapsular pressure, which is normalized at a time when kidney volume is still considerably increased. Renal blood flow and urinary kinin excretion are enhanced parallel to kidney volume. Renal prostaglandin E activity decreases. The increase in renal blood flow and urinary kinin excretion are inhibited by indomethacin pretreatment. The results leads to the conclusion that the kinins mediate the vascular response of bumetanide. The results also suggest that the subcapsular/interstitial pressure might affect the prostaglandin level of activity after bumetanide while factors related to tubular volume activate the kallikrein-kinin system.
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Uffe Bang Olsen (1977) studied this question.
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