Journal of Yeungnam Medical Science

Original Article

Effects of Cyclooxygenase Inhibitors on Vascular Reactivity and Alterations of Cyclooxygenase Expression.: Ki Young Lee, Jin Woo Park, Eun A Eum, Young Jin Kang, Kwang Youn Lee, Hyoung Chul Choi; Yeungnam Univ J Med. 2006;23(1):36-44. Published online June 30, 2006; DOI: https://doi.org/10.12701/yujm.2006.23.1.36

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Abstract PDF: BACKGROUND
There is controversy regarding whether COX-2 specific inhibitors are associated with elevation of blood pressure. We compared the effects of aspirin, indomethacin, and celecoxib for vascular reactivity induced by phenylephrine. We also tested the effects of indomethacin and NO donor on COX-1 and COX-2 protein expression, as well as nitrite production in culture medium of vascular smooth muscle cells. MATERILAS AND METHODS: In this experiment, we used the isometric tension study for vascular reactivity. After 45 minutes of pretreatment with aspirin, indomethacin, celecoxib, and phenylephrine induced contractions were tested. COX-1 and COX-2 protein expressions were analyzed by Western blot and nitrite production by the Griess reaction. RESULTS: Although celecoxib pretreatment caused enhanced arterial contraction, aspirin pretreatment induced more potent arterial contraction than celecoxib in the isometric tension study of rabbit femoral artery. COX-1 protein expression was unchanged by indomethacin, SNP and NOR-3; COX-2 protein expression was increased by the addition of indomethacin, SNP, and NOR-3. Especially, NOR-3, a NO donor, significantly increased COX-2 protein expression with unstimulated conditions as well as LPS stimulation. Induction of nitrite production was higher with NOR-3 treatment than SNP treatment with LPS stimulation. CONCLUSION: These results suggest that aspirin caused more potent vascular contraction than celecoxib and indomethacin. COX-2 expression in VSMC depended on the types of NO donor and LPS stimulation.

Review

Nonsteroidal Anti-inflammatory Drugs.: Choong Ki Lee; Yeungnam Univ J Med. 2000;17(1):1-11. Published online June 30, 2000; DOI: https://doi.org/10.12701/yujm.2000.17.1.1

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Abstract PDF: Inhibition of cyclooxygenase(COX), and thus prevention of the formation of prostaglandins, provided a unifying explanation of the therapeutic and toxic actions of nonsteroidal anti-inflammatory drugs(NSAIDs). Recently, the discovery of the two isoforms of COX was made by molecular biologists studying neoplastic transformation in chick embryo cells. The constitutive enzyme, COX-1, is obviously responsible for the production of prostaglandins involved in housekeeping functions such as maintenance of integrity of the gastric mucosa, renal blood flow and platelet aggregation. The inducible form of COX(COX-2) is responsible for the formation of prostaglandins that pathologic effects of inflammation, pain and fever. Clearly, all the experimental and clinical data support the hypothesis that the beneficial effects of NSAIDs are due to inhibition of the COX-2 enzyme, whereas the gastrotoxicity is due to inhibition of COX-1. The COX-2/COX-1 ratios of the NSAIDs in common use have been measured and compared with epidemiological data on their side effects. there is little evidence to suggest that one NSAID is clearly more efficacious than another and substantial individual variability is present with respect to the pharmacology and pharmacokinetics of these drugs, it is essential to adjust the dosage and choose specific drug to the patient`s response.

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