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Early renal post‐ischaemic tissue damage and dysfunction with contribution of A 1 ‐adenosine receptor activation in rat
Author(s) -
MOOSAVI SMS,
BAYAT G,
OWJI SM,
PANJEHSHAHIN MR
Publication year - 2009
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.2008.01024.x
Subject(s) - medicine , excretion , fractional excretion of sodium , renal function , endocrinology , renal ischemia , kidney , renal physiology , adenosine , reabsorption , adenosine receptor antagonist , renal blood flow , renal sodium reabsorption , ischemia , adenosine receptor , creatinine , adenosine a1 receptor , reperfusion injury , receptor , agonist
SUMMARY Aim: This study investigated the effect of a selective A 1 ‐adenosine receptor (A 1 ‐AR) antagonist, 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX), on the renal dysfunction and histological damage induced by ischaemia/reperfusion at an early stage. Methods: Pentobarbital anaesthetised rats were prepared for measuring renal functional variables. Ischaemia was induced by bilateral renal artery clamping for 30 min followed by a 4 h reperfusion period. In DPCPX‐treated rats, it was infused (i.v.) at 10 µg/kg per min before and after renal ischaemia. Both kidneys were examined using light and electron microscopy. Results: The renal ischaemic challenge resulted in major histological and ultrastructural damages, which were associated with decreased creatinine clearance, absolute potassium‐excretion and effective free‐water reabsorption, but increased fractional sodium‐excretion and urine flow during reperfusion period. In DPCPX‐treated rats, the histological and ultrastructural damage to the kidneys was improved along with the decrease in creatinine clearance and increase in fractional sodium‐excretion being smaller, but the increase in urine flow being larger than those of the non‐treated rats, while absolute potassium‐excretion and effective free‐water reabsorption were equal to those of the sham‐operated rats. Conclusion: These findings suggest that endogenous activation of A 1 ‐AR contributes to the early development of renal ischaemia/reperfusion injury.