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Organic nitrate metabolism

Fung and colleagues examined the metabolic conversion of organic nitrates in sub-cellular fractions of bovine coronary artery smooth muscle cells [66, 67]. They found NO-generating capacity to be present in membrane fractions and, with the use of marker enzymes, identified plasma membrane as the primary location. The enzyme involved in bioconversion was not glutathione-S-transferase [68] and differed from those that catalyse activation of organic nitrites [69]. Partial purification [70] established that the molecular sizes of the native enzyme and subunits were approximately 200 kDa and 58 kDa respectively, and that enzymic activity depends on the presence of a free thiol group. [Pg.38]

As mentioned earlier, the therapeutic use of organic nitrites [4] actually predates that of organic nitrates [1], Clinical utilisation of nitrites has, however, been very much less and this is reflected in the relatively sparse attention given to their mechanisms of action. Alkyl nitrites react readily with thiols to form S-nitrosothiols [122], which show biological effects similar to those of NO [11]. Nevertheless, glutathione-S-transferase has been implicated in the metabolism of organic nitrites, via intermediate... [Pg.44]

S-Nitroso derivatives of the biological thiols—glutathione, cysteine (115) and homocysteine—have been considered as bioactive intermediates in the metabolism of organic nitrates and the endothelium-derived relaxing factor with properties of nitric oxide. A simple, rapid and reproducible method for separating these thiols from their... [Pg.1149]

Fedisdi M (1991) Ihe action and metabolism of organic nitrates and their similarity with endothelium-derived rdaxing fa (EDRF). hi Moncada S, Higgs EA, Berrazueta IR eds. Clinical rdevance of nitric oxide in the cardiovascular system, Edioomplet Madrid, pp. 29-43... [Pg.471]

Sildenafil is contraindicated in patients who are taking organic nitrates, for their metabolism is blocked and severe and acute hypotension result. Patients with recent stroke or myocardial infarction or whose blood pressure is known to be < 90/50 mmHg should not use it. Sildenafil is a substrate for the P450 isoenzyme CYP3A4 (and to a lesser extent CYP2C9) which gives scope for interaction with inhibitors or inducers of this system. The metabolic inhibitors erythromycin, saquinavir and ritonavir (protease inhibitors used for AIDS), and cimetidine, for example, produce substantial rises in the plasma concentration of sildenafil. [Pg.545]


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