Isolated kidney preparations (IPK) from male Sprague Dawley rats perfused at constant pressure were used to evaluate the effect of angiotensin II (AII) and platelet-activating factor (PAF) on renal function and urinary protein excretion. Compared with basal, intrarenal infusion of AII at 8 ng/min caused a progressive increase in protein excretion (11 ± 6 versus 73 ± 21 μg/min) in parallel with a decline in renal perfusate flow (RPF) (29 ± 3 versus 18 ± 3 ml/min). Addition to the perfusate of PAF at 50 nM final concentration also induced proteinuria (9 ± 4 versus 55 ± 14 μg/min) but did not change RPF (29 ± 3 versus 30 ± 3 ml/min). Preexposure of isolated kidneys to the PAF receptor antagonist WEB 2086 prevented the increase in urinary protein excretion induced by AII infusion (basal: 13 ± 6; post-AII: 12 ± 7 μg/min) but failed to prevent the vasoactive effect of AII (RPF, basal: 30 ± 2; post-AII: 21 ± 3 ml/min). In additional experiments, dexamethasone reduced the proteinuric effect of PAF remarkably. These results indicate that in isolated kidney preparation: (1) AII infusion induced proteinuria and decreased RPF; and (2) the effect of AII in enhancing urinary protein excretion was completely prevented by a specific PAF receptor antagonist, which, however, did not influence the AII-induced fall in RPE. It is suggested that PAF plays a major role in AII-induced changes in the permselective function of the glomerular capillary barrier.
|Number of pages||8|
|Journal||Journal of the American Society of Nephrology|
|Publication status||Published - Sep 1997|
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