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首页> 外文期刊>Life sciences >Hypertension alters the participation of contractile prostanoids and superoxide anions in lipopolysaccharide effects on small mesenteric arteries.
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Hypertension alters the participation of contractile prostanoids and superoxide anions in lipopolysaccharide effects on small mesenteric arteries.

机译：高血压改变了收缩性前列腺素和超氧阴离子参与小肠系膜动脉脂多糖的作用。

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The involvement of cyclooxygenase-2 (COX-2)-derived products and superoxide anion in the effect of lipopolysaccharide in noradrenaline (NA)-induced contraction was investigated in small mesenteric arteries (SMA) from normotensive, Wistar Kyoto (WKY), and spontaneously hypertensive (SHR) rats. In WKY, lipopolysaccharide (10 &mgr;g/ml, 1 and 5 h) only inhibited the NA response (0.1-30 &mgr;M) in the presence of dexamethasone (1 &mgr;M), indomethacin (10 &mgr;M), the selective COX-2 inhibitor, NS 398 (10 &mgr;M), and the TXA(2)/PGH(2) receptor antagonist, SQ 29,548 (10 &mgr;M) but not of superoxide dismutase (SOD, 100 U/ml). In SHR, lipopolysaccharide inhibited the NA response by itself; this inhibition was potentiated by dexamethasone, indomethacin, NS 398, SQ 29,548 and SOD. The effect of lipopolysaccharide plus indomethacin, NS 398 or SQ 29,548 was higher in SMA from WKY than SHR only after 1 h lipopolysaccharide incubation. N(G)-nitro-L-arginine methyl ester (100 &mgr;M) and endothelium removal abolished the indomethacin-induced potentiatory effect of lipopolysaccharide in both strains. Endothelium removal also abolished the SOD potentiatory effect in SMA from SHR. Lipopolysaccharide increases COX-2 expression to a similar level in both strains and iNOS expression in a greater extent in SHR; these increases were reduced by dexamethasone. These results indicate: 1) lipopolysaccharide induces the endothelial production of contractile prostanoids from COX-2 in SMA, probably to compensate the increase in NO from iNOS; 2) the production of prostanoids in the presence of lipopolysaccharide seems to be greater in normotensive than hypertensive rats only after lipopolysaccharide short incubation times; 3) endothelial production of O(2)(z.rad;-) contributes to counteract depression of NA contraction caused by lipopolysaccharide only in SHR.
机译：在正常血压的小肠系膜动脉（SMA），Wistar Kyoto（WKY）的自发性肠系膜动脉（SMA）中，研究了环氧合酶2（COX-2）衍生的产物和超氧阴离子在去甲肾上腺素（NA）诱导的收缩中对脂多糖的影响。高血压（SHR）大鼠。在WKY中，脂多糖（10 g / ml，1和5 h）仅在地塞米松（1 mg），消炎痛（10 mg）的存在下抑制NA反应（0.1-30 mg），选择性COX-2抑制剂NS 398（10μM）和TXA（2）/ PGH（2）受体拮抗剂SQ 29,548（10μM），但不是超氧化物歧化酶（SOD，100 U / ml） ）。在SHR中，脂多糖本身抑制了NA反应。地塞米松，消炎痛，NS 398，SQ 29,548和SOD可增强这种抑制作用。仅在脂多糖孵育1小时后，来自WKY的SMA中脂多糖加消炎痛，NS 398或SQ 29,548的作用高于SHR。 N（G）-硝基-L-精氨酸甲酯（100μM）和内皮去除消除了吲哚美辛诱导的两种菌株中脂多糖的增强作用。去除内皮还消除了SHR对SMA的SOD增强作用。在SHR中，脂多糖将两种菌株中的COX-2表达增加到相似的水平，而iNOS的表达则在更大程度上增加。地塞米松减少了这些增加。这些结果表明：1）脂多糖可诱导SMA中COX-2产生内皮型收缩性前列腺素，可能是补偿iNOS引起的NO升高。 2）在脂多糖存在下，仅在脂多糖孵育时间短后，在正常血压情况下，在脂多糖存在下前列腺素的产生似乎比高血压大鼠要大。 3）O（2）（z.rad ;-)的内皮生成有助于抵消仅在SHR中由脂多糖引起的NA收缩的降低。

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