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

Role of acid sphingomyelinase and IL-6 as mediators of endotoxin-induced pulmonary vascular dysfunction

“…Thus, incubation with IL-6 (30 ng/mL; concentration within the range produced by PASMCs upon LPS challenge) increased the contractile responses to serotonin, inhibited HPV and reduced the relaxant responses to acetylcholine in isolated PAs, thereby mimicking the effects of LPS. Induction of endothelial dysfunction by IL-6 has been shown in other vascular beds,44 45 through a mechanism involving inhibition of Akt and stabilisation of interactions between endothelial NOS and caveolin 1 46 47. However, in contrast to the effects observed in systemic arteries,48 IL-6 did not reduce the contractile responses to phenylephrine but potentiated those induced by serotonin in isolated rat PAs.…”

The effect of endothelin‐1 on the production of interleukin‐6 in cultured human detrusor smooth muscle cells, and the effect of interleukin‐6 on the contractile response of bladder smooth muscle strips from rats

“…IL‐6 also potentiated the ET‐1‐induced vascular perfusion pressure [7]. Recently, we reported that the contractile responses to phenylephrine were significantly greater in IL‐6‐treated cavernosal strips of rat than untreated strips, and the relaxation responses to ACh were significantly lower in the IL‐6‐treated group than in the untreated group [9].…”

“…By contrast, electrical‐field stimulation‐induced acetylcholine (ACh) release was significantly reduced in IL‐6‐treated oesophageal strips [8]. Recently, we reported that IL‐6 inhibited endothelium‐dependent, nitric oxide‐mediated relaxation and enhanced α 1 ‐adrenergic receptor‐mediated contraction in the cavernosal SM strips from rats [9]. Considering these situations, we considered the possibility that ET‐1 produced in the bladder under conditions of BOO would induce a greater production of IL‐6 and a higher concentration of IL‐6 would lead to detrusor overactivity, and thus irritative symptoms of the bladder would be aggravated.…”

Interleukin-6 inhibits endothelial nitric oxide synthase activation and increases endothelial nitric oxide synthase binding to stabilized caveolin-1 in human vascular endothelial cells

“…Direct effect of a wide range of well defined cytokines on vascular tone in isolated human artery has been studied and IL-6 was demonstrated to induce the contraction of artery and this vascular effect was endothelium-dependent [19]. A recent work done by Myung et al [20] in 2008 reported that contractile response to phenylephrine was significantly enhanced in the IL-6-treated strip and the relaxation response to acetylcholine was significantly inhibited by IL-6. These effects were not observed after endothelial denudation, again suggesting an endotheliumdependent mechanism.…”