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Kinetics difference of regional sodium content change between medulla and cortex of kidney after furosemide injection
Author(s) -
Liu Haiying,
Kohler Martin G,
Shen Xiaolan,
Garcia Maria L,
AlonsoGalicia Maggie,
Priest Birgit T,
Williams Donwald S,
Hargreaves Richard,
Kaczorowski Gregory J
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.968.22
Subject(s) - furosemide , sodium , chemistry , medulla , kinetics , kidney , cortex (anatomy) , endocrinology , renal cortex , medicine , biophysics , anatomy , biology , neuroscience , physics , organic chemistry , quantum mechanics
3D sodium images of living rat kidneys were obtained at 9.4 Tesla to track its regional kinetics in response to diuretics. In each experiment, diuretics infusion was started when the stable physiological condition was achieved under anesthesia (isofluorane), during which sodium images were continuously collected. Initial results showed that there existed a large corticomedullary sodium gradient under normal physiological condition and after administration of furosemide (6ug/min, BW=300g) this gradient was significantly attenuated within 10min. Also, we found that the sodium content collapsed much more quickly in medulla than in cortex, with characteristic time constants: 8.4+/−4.3 and 95+/−25mins (p<0.0027). Corresponding normalized changes of sodium signals in medullar and cortical regions are found to be: −0.71+/−0.02 and 1.41+/−0.07. In conclusion, in vivo experiments using furosemide given at clinically relevant doses through relatively slow infusion have revealed that sodium contents in medullary and cortical regions of rat kidney exhibited different temporal kinetics. These results are consistent with the mechanism of action of furosemide, i.e. inhibition of Na/K/2Cl co‐transporter in the thick ascending limb of Henle, which is responsible for establishing and maintaining a large sodium gradient across the kidney in the corticomedullary direction.