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首页> 外文期刊>Life sciences >Nitric oxide-dependent and -independent inhibition by lipopolysaccharide of phosphoinositide hydrolysis in vascular smooth muscle.
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Nitric oxide-dependent and -independent inhibition by lipopolysaccharide of phosphoinositide hydrolysis in vascular smooth muscle.

机译：脂多糖对一氧化氮的依赖性和非依赖性对血管平滑肌中磷酸肌醇水解的抑制作用。

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The present study was designed in order to clarify the mechanisms of diminished phosphoinositide (PI) hydrolysis by lipopolysaccharide (LPS) in blood vessels. In vitro pretreatment of rat aortic strips with LPS (1 microg/ml) for 10 or 24 hrs inhibited 5-hydroxytryptamine (5-HT, 100 microM)-induced inositol monophosphate accumulation in a time-dependent manner. Coincubation of the aortas with N(G)-monomethyl-L-arginine (LNMMA, 1 mM) completely prevented the early diminution of 5-HT-stimulated PI hydrolysis after 10-hr exposure to LPS but did not affect the delayed diminution after 24-hr exposure. Coincubation with cycloheximide (1 microM) did not prevent the delayed LPS-induced diminution of phosphoinositide hydrolysis. Tetraethylammonium (10 mM) did not restore the diminished phosphoinositide hydrolysis after 24-hr exposure to LPS, suggesting that the diminution is not due to K+ channel activation. Sodium fluoride (10 mM)-induced inositol monophosphate accumulation was also decreased in the aortic strips after LPS incubation for 24 hrs, and this decrease was not prevented by coincubation with LNMMA. LPS incubation time-dependently increased nitric oxide (NO) production in the aortas, which was completely inhibited by LNMMA or cycloheximide. These results suggest that NO is mainly involved in the inhibitory action of LPS on stimulated-PI hydrolysis in the early stage, while in the later stage, a factor(s) besides NO causes attenuation of the stimulated-PI hydrolysis.
机译：本研究旨在阐明血管中脂多糖（LPS）水解磷酸肌醇（PI）减少的机制。用LPS（1 microg / ml）对大鼠主动脉条进行体外预​​处理10或24小时，以时间依赖性方式抑制了5-羟色胺（5-HT，100 microM）诱导的肌醇单磷酸酯积累。将主动脉与N（G）-单甲基-L-精氨酸（LNMMA，1 mM）共同孵育可完全防止LPS暴露10小时后5-HT刺激的PI水解的早期减少，但不影响24小时后的延迟减少-hr曝光。与环己酰亚胺（1 microM）共同孵育不能防止LPS诱导的磷酸肌醇水解减少。在暴露于LPS 24小时后，四乙铵（10 mM）不能恢复减弱的磷酸肌醇水解，这表明这种减少不是由于K +通道激活引起的。 LPS孵育24小时后，主动脉带中氟化钠（10 mM）诱导的肌醇单磷酸积累也减少了，与LNMMA共孵育不能阻止这种减少。 LPS孵育时间依赖性地增加了主动脉中一氧化氮（NO）的产生，这被LNMMA或环己酰亚胺完全抑制。这些结果表明，NO在早期主要参与LPS对PI刺激的水解的抑制作用，而在后期，除了NO之外，还有其他因素导致PI刺激的水解减弱。

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