Oxidant stress and glomerular prostanoid production: influence of angiotensin converting enzyme inhibition.
1. The effect of H2O2 (4.7 x 10(-9) -4.7 x 10(-3) M) on prostanoid production by isolated glomeruli from normotensive (WKY) and, spontaneously hypertensive rats (SHR) has been studied. 2. Oxidant stress significantly increased synthesis of prostaglandin E2 (PGE2), I2 (PGI2) and thromboxane A2 (TxA2) by glomeruli from both strains whereas the ratio (PGE2 + PGI2)/TxA2 increased in only SHR. 3. Pre-incubation of glomeruli with the angiotensin converting enzyme inhibitors captopril or lisinopril, had virtually no effect on H2O2-induced synthesis of individual prostanoids nor on the ratio (PGE2 + PGI2)/TxA2 by glomeruli from either WKY or SHR. 4. The findings suggest that H2O2-induced changes in glomerular function may be mediated, in part, by PGs but fail to support the suggestion that the ability of ACEI to protect glomeruli from H2O2-induced damage is determined by PGs.
Renal Laboratory, School of Postgraduate Medicine, University of Keele, England.
L
L
Clayton
C
C
Hiley
R J
RJ
D'Souza
P W
PW
Jones
S J
SJ
Davies
R C
RC
Strange
G M
GM
Aber
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D015232:Dinoprostone / Q000096:biosynthesis; D004151:Dipeptides / Q000494:pharmacology; D011464:Epoprostenol / Q000096:biosynthesis; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D007678:Kidney Glomerulus / Q000187:drug effects / Q000378:metabolism*; D017706:Lisinopril; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013928:Thromboxane A2 / Q000096:biosynthesis
D000806:Angiotensin-Converting Enzyme Inhibitors; D004151:Dipeptides; D011453:Prostaglandins; D013928:Thromboxane A2; D002216:Captopril; D006861:Hydrogen Peroxide; D011464:Epoprostenol; D017706:Lisinopril; D015232:Dinoprostone