Why the study?
Does bumetanide alter renal compliance, prostaglandin, and kinin activity in anaesthetized dogs?
Does bumetanide alter renal compliance, prostaglandin, and kinin activity in anaesthetized dogs?
Bumetanide-induced increases in renal blood flow and urinary kinin excretion in dogs are mediated by kinins and inhibited by indomethacin.
Findings in anaesthetized dogs should not alter bumetanide use; leaves open kinin-prostaglandin mediation of renal effects for translational 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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