title: [Role of nitric oxide in cholecystokinin  octapeptide alleviation of tumor necrosis factor  alpha induced changes in rabbit pulmonary arterial reactivity].
abstract: To explore the mechanism underlying cholecystokinin octapeptide (CCK-8) induced attenuation in pulmonary arterial hypertension (PAH) in endotoxic shock (ES), the effect of CCK-8 on the changes in rabbit pulmonary arterial reactivity induced by tumor necrosis factor-alpha (TNF-alpha) was observed with isolated arterial ring technique and by examination of nitric oxide synthase (NOS). The contractile response to 10(-6) mol/L phenylephrine (PE) and the endothelium dependent relaxation response to 10(-6) mol/L acetylcholine (ACh) were not affected by TNF-alpha (4000 U/ml) after incubation for 2 h; the relaxation response was decreased significantly when the incubation was prolonged to 7 or 14 h, which, however, could be reversed by a concomitant exposure to CCK-8 (0.5 microgram/ml), but the incubation of pulmonary arterial rings with CCK-8 (0.5 microgram/ml) alone did not bring out any contractile responses. The endothelium dependent relaxation response to 10(-6) mol/L ACh was restored by L arginine in the TNF-alpha group which had been incubated for 7 h, but was not affected by AG in each group, while the contractile response to 10(-6) mol/L PE increased significantly in the TNF-alpha group. The relaxant response to 10(-6) mol/L ACh changed into a contractile response after preincubation with L-NNA in each group, while the contraction response to 10(-6) mol/L PE increased significantly. The NOS activity increased in the TNF-alpha and the TNF alpha+CCK-8 groups, while no significant difference was observed between the vehicle and the CCK-8 groups. These results suggest that CCK-8 prevents TNF-alpha induced impairment in endothelium dependent relaxation response, and the effects of both CCK-8 and TNF-alpha are related to NO.
authors.affiliation: Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: A H
authors.initials: AH
authors.lastname: Meng
authors.forename: Y L
authors.initials: YL
authors.lastname: Ling
authors.forename: D H
authors.initials: DH
authors.lastname: Wang
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Gu
authors.forename: S J
authors.initials: SJ
authors.lastname: Li
authors.forename: T N
authors.initials: TN
authors.lastname: Zhu
mesh_terms: D000818:Animals; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D009569:Nitric Oxide / Q000502:physiology*; D011651:Pulmonary Artery / Q000187:drug effects / Q000502:physiology*; D011817:Rabbits; D012844:Sincalide / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D012844:Sincalide