Angiotensin II modulates glomerular capillary permselectivity in rat isolated perfused kidney.
Author(s) -
Radosław Łapiński,
Norberto Perico,
Andrea Remuzzi,
Fabio Sangalli,
Ariela Benigni,
Giuseppe Remuzzi
Publication year - 1996
Publication title -
journal of the american society of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.451
H-Index - 279
eISSN - 1533-3450
pISSN - 1046-6673
DOI - 10.1681/asn.v75653
Subject(s) - ficoll , medicine , renal function , endocrinology , chemistry , renin–angiotensin system , kidney , angiotensin ii , excretion , urinary system , receptor , biochemistry , blood pressure , in vitro , peripheral blood mononuclear cell
Studies in experimental animals and humans have documented that inhibition of the renin-angiotensin system by angiotensin-converting enzyme inhibitors reduces urinary protein excretion rate and retards the development of renal injury. Here we sought to investigate whether angiotensin II (All) modified the size-selective properties to macromolecules of the glomerular capillary barrier in isolated perfused rat kidney preparation. Compared with basal values, continuous All infusion into the renal artery at the rate of 3 or 8 ng/min, but not at 0.6 ng/min, induced a progressive and significant increase in urinary protein excretion rate. Evaluation of the sieving properties of the glomerular barrier by fractional clearance of polydisperse Ficoll showed that All significantly enhanced the filtration of tracer molecules of radil > or = 34A. All-induced changes in urinary protein excretion rate and in Ficoll fractional clearance were completely prevented by pretreatment with the specific All Type 1 receptor antagonist SR 47436.
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