Uses
Bumetanide sodium, a highly potent loop diuretic, is a Na+-K+-Cl+ cotransporter (NKCC) blocker. Bumetanide sodium is a selective NKCC1 inhibitor, and also inhibits NKCC2, with IC50s of 0.68 and 4.0 μM for hNKCC1A and hNKCC2A, respectively[1][2].
in vivo
Bumetanide sodium (7.6-30.4 mg/kg; i.v.) attenuates the decrease in apparent diffusion coefficients (ADC) ratios for both cortex and striatum (by 40-67%), indicating reduced edema formation[3].
Bumetanide sodium also reduces infarct size[3].
Bumetanide sodium shows different half-lives of 21.4 min, 53.8 min and 137 min following 2 mg/kg, 8 mg/kg and 20 mg/kg intravenous injection, respectively, in rats[4].
References
[1] Lykke K, et al. The search for NKCC1-selective drugs for the treatment of epilepsy: Structure-function relationship of bumetanide and various bumetanide derivatives in inhibiting the human cation-chloride cotransporter NKCC1A. Epilepsy Behav. 2016 Jun;59: DOI:
10.1016/j.yebeh.2016.03.021[2] Ciaran Richardson, et al. Regulation of the NKCC2 ion cotransporter by SPAK-OSR1-dependent and -independent pathways. J Cell Sci. 2011 Mar 1;124(Pt 5):789-800. DOI:
10.1242/jcs.077230[3] Martha E O'Donnell, et al. Bumetanide inhibition of the blood-brain barrier Na-K-Cl cotransporter reduces edema formation in the rat middle cerebral artery occlusion model of stroke. J Cereb Blood Flow Metab. 2004 Sep;24(9):1046-56. DOI:
10.1097/01.WCB.0000130867.32663.90[4] S H Lee, et al. Pharmacokinetics and pharmacodynamics of bumetanide after intravenous and oral administration to rats: absorption from various GI segments. J Pharmacokinet Biopharm. 1994 Feb;22(1):1-17.6 DOI:
10.1007/BF02353407
