OBJECTIVETo explore the effect and mechanism of iron on the vasodilating effect of interleukin-2 (IL-2) in the isolated aortic ring.

METHODSIsometric tension was recorded in response to drugs in organ bath. Ferric ammonium citrate (FAC) was added to the bath 30 min before phenylephrine (1 micromol/L), which was followed by IL-2 in a cumulative fashion. Spectrophotometry was used to determine the activity of nitric oxide synthase (NOS) of the thoracic aorta.

RESULTSFAC (0.1 - 10 micromol/L) alone did not affect the tension of rings,but inhibited the vasodilating effect of IL-2 (1 - 1,000 U/ml) in a dose dependent manner. IL-2(1, 10, 100, 1000 U/ml) decreased the aortic tension to (78.47+/-4.31)%, (66.86+/-5.55)%, (52.62+/-4.51)% and (42.39+/-4.27)% of pre-drug control, respectively. However, after incubation with 10 micromol/L FAC in the presence of IL-2, the aortic tension was reduced to (89.81+/-1.94)%, (86.13+/-3.11)%, (77.16+/-5.66)% and (68.76+/-5.69)% of pre-drug control, respectively. Pretreatment with L-arginine (1 mmol/L) abolished the inhibitory effect of FAC. Pretreatment with FAC attenuated the increased activity of NOS induced by IL-2 from (22.10+/-1.87)U/mg prot to (15.71+/-0.89)U/mg prot. High Ca(2+) (2.5 mmol/L) incubation did not change the inhibitory effect of FAC. Pretreatment with FAC attenuated the increased caffeine-releasable pool of Ca(2+) by IL-2. High K(+) (10 mmol/L) incubation abolished the inhibitory effect of FAC.

CONCLUSIONFAC inhibits the vasodilating effect of IL-2 in the isolated aortic ring,which may be mediated by decreasing the activity of NOS. Intracellular calcium release and inward rectifier potassium channel are involved in the inhibitory effect of FAC.