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  • Title: Lack of evidence for the involvement of cytochrome P-450 or other hemoproteins in metabolic activation of glyceryl trinitrate in rabbit aorta.
    Author: Liu Z, Brien JF, Marks GS, McLaughlin BE, Nakatsu K.
    Journal: J Pharmacol Exp Ther; 1993 Mar; 264(3):1432-9. PubMed ID: 8450477.
    Abstract:
    The present study was conducted to test the hypothesis that glyceryl trinitrate (GTN) metabolic activation in blood vessels is mediated by cytochrome P-450 or some other hemoprotein. The effects of cytochrome P-450 inhibitor [2-dimethylaminoethyl-2,2-diphenyl-n-pentanoate (SKF-525A) and metyrapone] on the response of rabbit aortic rings to GTN was determined by recording cumulative GTN dose-response curves in the presence of either or both inhibitors. The cytochrome P-450 inhibitors did not interfere with the ability of GTN to relax rabbit aortic rings. Treatment of rabbit aortic strips (RAS) with carbon monoxide (CO) was undertaken to elucidate a potential role of ferrous hemoproteins in mediating GTN-induced relaxation. CO did not significantly inhibit GTN-induced vasodilation of RAS. Biotransformation of GTN to glyceryl dinitrates by RAS exposed to CO for 5 min or nitric oxide (NO) for 10 min was determined by incubation of the tissues with 0.5 microM [3H]- or [14C]-GTN in the presence of CO or NO for 10 sec, 30 sec or 2 min. Neither CO nor NO exposure inhibited glyceryl-1,2- or -1,3-dinitrate formation by RAS after the 10-sec or 2-min incubation with RAS. For the 30-sec incubation, NO exposure did inhibit glyceryl dinitrate formation by RAS. This was deemed to be less important than the 10-sec data, the time just before the onset of relaxation. Therefore, emphasis is placed on lack of inhibition by NO at this earlier time point.(ABSTRACT TRUNCATED AT 250 WORDS)
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