Hypertension alters the participation of contractile prostanoids and superoxide anions in lipopolysaccharide effects on small mesenteric arteries

Ana M. Briones, María J. Alonso, Raquel Hernanz, Silvia Tovar, Elisabet Vila, Mercedes Salaices

Research output: Contribution to journalArticleResearchpeer-review

22 Citations (Scopus)

Abstract

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 μg/ml, 1 and 5 h) only inhibited the NA response (0.1-30 μM) in the presence of dexamethasone (1 μM), indomethacin (10 μM), the selective COX-2 inhibitor, NS 398 (10 μM), and the TXA2/PGH2 receptor antagonist, SQ 29,548 (10 μM) 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. NG-nitro-L-arginine methyl ester (100 μM) 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 O2·- contributes to counteract depression of NA contraction caused by lipopolysaccharide only in SHR. © 2002 Elsevier Science Inc. All rights reserved.
Original languageEnglish
Pages (from-to)1997-2014
JournalLife Sciences
Volume71
DOIs
Publication statusPublished - 13 Sep 2002

Keywords

  • COX-2
  • Hypertension
  • Lipopolysaccharide
  • Noradrenaline
  • Rat small mesenteric arteries
  • Reactive oxygen species

Fingerprint

Dive into the research topics of 'Hypertension alters the participation of contractile prostanoids and superoxide anions in lipopolysaccharide effects on small mesenteric arteries'. Together they form a unique fingerprint.

Cite this