Dexamethasone inhibits interleukin-lβ induced smooth muscle oscillation by a mechanism not involving nitric oxide

T. S. Yoon, J. S. Jin, R Clinton Webb, L. G. D'Alccy

Research output: Contribution to journalArticlepeer-review


Agonist-induced smooth muscle oscillations occur in vessels incubated in interleukin-lβ. The induction of inducible isoform of nitric oxide synthase (iNOS) by interleukin- IB can be inhibited by dexamethasone. We tested the hypothesis that interleukin-lβ induced oscillation is mediated by iNOS and dexamethasone eliminates oscillation by inhibiting that induction. Rat aortic rings were incubated with interleukin-IB (10 ng/ml). Some of the rings were incubated with dexamethasone (10-6 M) plus interleukin-IB. After incubation, the aortic rings were mounted in a tissue bath for isometric tension recording. Oscillations were observed during cumulative phenylephrine contractile responses, and during relaxation induced by Larginine in phenylephrine precontracted rings. Dexamethasone significantly inhibited oscillation magnitude and frequency during the above periods. In contrast, the maximal oscillation force and frequency during the phenylephrine contractile period were significantly increased by pretreatment with Nω-nitro-L-arginine (an iNOS inhibitor) in 7 hour interleukin-IB incubated vessels. This suggests that the activity of iNOS is not required during agonist-induced oscillations despite the fact that 7 hour incubation with dexamethasone + interleukin-lβ significantly inhibited L-arginine induced relaxation (indicator of iNOS activity). The decreasing oscillation activity in interleukin-1 βincubated vessels by dexamethasone may be mediated through mechanisms other than inhibiting iNOS.

Original languageEnglish (US)
JournalFASEB Journal
Issue number3
StatePublished - Dec 1 1996

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics


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