Key result
Glyceryl trinitrate bioactivation relies on the aldehyde dehydrogenase enzyme, with reduced efficacy observed in subjects carrying the Glu504Lys mutation.
Why the study?
Despite GTN's central role as an angina treatment and NO-donating compound, establishing the precise mechanism of its medicinal benefit and nitrate tolerance has proven difficult.
Healthcare professionals should be aware that patients with alcohol intolerance due to ALDH mutations may experience reduced efficacy when administered GTN for emergency treatment.
GTN pathway update informs NO biology; extends mechanistic insights but leaves open clinical optimization.
Glyceryl trinitrate (GTN) is one of the earliest known treatments for angina with a fascinating history that bridges three centuries. However, despite its central role in the nitric oxide (NO) story as a NO-donating compound, establishing the precise mechanism of how GTN exerts its medicinal benefit has proven to be far more difficult. This review brings together the explosive and vasodilatory nature of this three-carbon molecule while providing an update on the likely in vivo pathways through which GTN, and the rest of the organic nitrate family, release NO, nitrite, or a combination of both, while also trying to explain nitrate tolerance. Over the last 20 years the alcohol detoxification enzyme, aldehyde dehydrogenase (ALDH), has undoubtedly emerged as the front runner to explaining GTN's bioactivation. This is best illustrated by reduced GTN efficacy in subjects carrying the single point mutation (Glu504Lys) in ALDH, which is also responsible for alcohol intolerance, as characterized by flushing. While these findings are significant for anyone following the GTN story, they appear particularly relevant for healthcare professionals, and especially so, if administering GTN to patients as an emergency treatment. In short, although the GTN puzzle has not been fully solved, clinical study data continue to cement the importance of ALDH, as uncovered in 2002, as a key GTN activator.
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Pearson et al. (2021) conducted a review in Angina. Glyceryl trinitrate (GTN) was evaluated. Glyceryl trinitrate bioactivation relies on the aldehyde dehydrogenase enzyme, with reduced efficacy observed in subjects carrying the Glu504Lys mutation.
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