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Role of carbonic anhydrase in acute recovery following renal ischemia reperfusion injury
Author(s) -
Nensén Oskar,
Hansell Peter,
Palm Fredrik
Publication year - 2017
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.31.1_supplement.1030.8
Subject(s) - acetazolamide , ischemia , renal function , kidney , renal ischemia , carbonic anhydrase , renal sodium reabsorption , renal blood flow , acute kidney injury , pharmacology , chemistry , medicine , endocrinology , excretion , urinary system , reperfusion injury , biochemistry , enzyme , reabsorption
Ischemia reperfusion injury is a common cause of acute kidney injury in the clinic. It has previously been reported that kidney oxygen consumption (QO 2 ) in relation to glomerular filtration rate (GFR), and thus sodium load, is markedly increased following an ischemic insult. Since proximal tubular sodium transport (TNa) is a major contributor to overall QO 2 , we investigated how inhibition of TNa in this particular tubular segment impacted on oxygen metabolism and kidney function during the acute recovery following 45 minutes of warm ischemia by inhibiting carbonic anhydrase using acetazolamide. Male Sprague Dawley rats were anesthetized and administered acetazolamide (50 mg/kg; n=11) or volume‐matched vehicle (n=12). Kidney function, hemodynamics and QO 2 were determined before and after complete ischemia by clamping the renal artery. Acetazolamide per se reduced GFR (−20%) and TNa (−22%), while it increased urine flow (+91%) and urinary sodium excretion (+3600%). Renal blood flow was reduced (−31%) as a result of increased renal vascular resistance (+37%) but without affecting QO 2 . Ischemia reperfusion per se resulted in similar decrease in GFR, TNa, and TNa/QO 2 independently of carbonic anhydrase status. However, the QO 2 /GFR ratio following ischemia‐ reperfusion was profoundly increased in the group receiving carbonic anhydrase inhibition indicating a significant contribution of basal oxygen metabolism to the total kidney QO 2 following inhibition of proximal tubular function after an ischemic insult. Support or Funding Information Swedish Research Council ‐ Medicine and Health