Key result
Pre-incubation with ACE inhibitors captopril or lisinopril had virtually no effect on H2O2-induced synthesis of prostanoids by isolated glomeruli from normotensive or hypertensive rats.
Why the study?
Does pre-incubation with ACE inhibitors alter H2O2-induced prostanoid production in isolated rat glomeruli?
Does pre-incubation with ACE inhibitors alter H2O2-induced prostanoid production in isolated rat glomeruli?
ACE inhibitors do not appear to protect glomeruli from H2O2-induced damage via modulation of prostanoid synthesis.
ACE inhibitors do not modulate H2O2-induced prostanoid synthesis in rat glomeruli; leaves open alternative renoprotective mechanisms in vivo.
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.
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Clayton et al. (1993) studied Normotensive and spontaneously hypertensive rats (isolated glomeruli). H2O2 and ACE inhibitors (captopril or lisinopril) vs. No ACE inhibitor was evaluated on Prostanoid production (PGE2, PGI2, TxA2) and ratio (PGE2 + PGI2)/TxA2. Pre-incubation with ACE inhibitors captopril or lisinopril had virtually no effect on H2O2-induced synthesis of prostanoids by isolated glomeruli from normotensive or hypertensive rats.
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