http://linked.open...generalReferences
| - # Rais-Bahrami K, Majd M, Veszelovszky E, Short BL: Use of furosemide and hearing loss in neonatal intensive care survivors. Am J Perinatol. 2004 Aug;21(6):329-32. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/15311369 # Korpi ER, Kuner T, Seeburg PH, Luddens H: Selective antagonist for the cerebellar granule cell-specific gamma-aminobutyric acid type A receptor. Mol Pharmacol. 1995 Feb;47(2):283-9. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/7870036 # Tia S, Wang JF, Kotchabhakdi N, Vicini S: Developmental changes of inhibitory synaptic currents in cerebellar granule neurons: role of GABA(A) receptor alpha 6 subunit. J Neurosci. 1996 Jun 1;16(11):3630-40. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/8642407 # Wafford KA, Thompson SA, Thomas D, Sikela J, Wilcox AS, Whiting PJ: Functional characterization of human gamma-aminobutyric acidA receptors containing the alpha 4 subunit. Mol Pharmacol. 1996 Sep;50(3):670-8. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/8794909 (en)
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http://linked.open...mechanismOfAction
| - Furosemide, a loop diuretic, inhibits water reabsorption in the nephron by blocking the sodium-potassium-chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle. This is achieved through competitive inhibition at the chloride binding site on the cotransporter, thus preventing the transport of sodium from the lumen of the loop of Henle into the basolateral interstitium. Consequently, the lumen becomes more hypertonic while the interstitium becomes less hypertonic, which in turn diminishes the osmotic gradient for water reabsorption throughout the nephron. Because the thick ascending limb is responsible for 25% of sodium reabsorption in the nephron, furosemide is a very potent diuretic. (en)
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