The effects of interleukin-6 on the contraction and relaxation responses of the cavernous smooth muscle from rats

Eur J Pharmacol. 2008 Jul 28;589(1-3):228-32. doi: 10.1016/j.ejphar.2008.04.053. Epub 2008 May 5.


The purpose of this study is to elucidate the effect of IL-6 on the vasomotor reactivity of the corpus cavernosum of the rats. The strips were either left untreated or treated with 1 ng/ml of IL-6 for 60 min. By increasing concentrations of phenylephrine, acetylcholine, or sodium nitroprusside, we assessed concentration-contraction or relaxation responses. The IL-6-treated strips were incubated for 30 min with or without L-NAME (N(W)-nitro-L-arginine methyl ester), L-arginine, indomethacin, BQ-123 (an endothelin receptor A inhibitor), or SQ 29,548 (a thromboxane A(2) [TXA(2)] receptor blocker), and the effects on phenylephrine-induced contraction or acetylcholine-induced relaxation of phenylephrine-induced contraction were measured. The contractile responses to phenylephrine were significantly enhanced in the IL-6-treated strips, compared with the IL-6-nontreated strips, and the relaxation responses to acetylcholine were significantly inhibited in the IL-6-treated group compared with the IL-6-nontreated group. But after endothelial denudation, there was no difference between the IL-6-treated strips and the IL-6-nontreated strips on the contraction-relaxation responses to phenylephrine or acetylcholine. The relaxation responses to sodium nitroprusside were not inhibited in both groups. L-NAME completely inhibited the relaxation response to acetylcholine in the IL-6-treated strips, as well as the IL-6-nontreated strips. Indomethacin and SQ 29,548 significantly inhibited the increased contractile responses to phenylephrine in the IL-6-treated strips. But BQ 123 rarely affected the same responses. L-arginine reversed the inhibited relaxation responses to acetylcholine in the IL-6-treated strips. Therefore, IL-6 inhibits endothelium-dependent, NO-mediated relaxation and also enhances alpha(1)-adrenergic receptor-mediated contraction via an endothelium-dependent TXA(2)-mediated mechanism in the corpus cavernosum of the rat.

MeSH terms

  • Animals
  • Cyclooxygenase Inhibitors / pharmacology
  • Dose-Response Relationship, Drug
  • Endothelins / metabolism
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / enzymology
  • Endothelium, Vascular / metabolism*
  • Enzyme Inhibitors / pharmacology
  • Interleukin-6 / metabolism*
  • Male
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitric Oxide Synthase / metabolism
  • Penis / blood supply*
  • Prostaglandin-Endoperoxide Synthases / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Adrenergic, alpha-1 / metabolism
  • Thromboxane A2 / metabolism
  • Vasoconstriction* / drug effects
  • Vasoconstrictor Agents / pharmacology
  • Vasodilation* / drug effects
  • Vasodilator Agents / pharmacology


  • Cyclooxygenase Inhibitors
  • Endothelins
  • Enzyme Inhibitors
  • Interleukin-6
  • Receptors, Adrenergic, alpha-1
  • Vasoconstrictor Agents
  • Vasodilator Agents
  • Nitric Oxide
  • Thromboxane A2
  • Nitric Oxide Synthase
  • Prostaglandin-Endoperoxide Synthases