Opposite effects of nicotinic acid and pyridoxine on systemic prostacyclin, thromboxane and leukotriene production in man

The effects of nicotinic acid (2500 mg orally during 12 hr) and pyridoxine (300 mg orally twice daily for seven days) on the excretion of urinary 2,3-dinor-6-ketoprostaglandin F1a, 11-dehydrothromboxane B2 and leukotriene E4, the markers of systemic prostacyclin, thromboxane A2 and cysteinyl leukotriene production, respectively, were investigated in healthy male volunteers (nΩ6-8). Nicotinic acid increased 11-dehydrothromboxane B2 and leukotriene E4 excretions to 2.6- and 2.0 times the initial values (P0.05), respectively. In the volunteers treated with pyridoxine, 11-dehydrothrombox- ane B2 and leukotriene E4 excretions were decreased to 70% (P0.05) and 65% (P0.01) of the initial values, respectively, but the excretion of 2,3-dinor-6-ketoprostaglandin F1a was increased 1.7 times (P0.01). The results suggest that nicotinic acid increases thromboxane and leukotriene synthesis which may not be beneficial for patients with cardiovascular diseases or asthma. In contrast, the increase in prostacyclin production and the inhibition in thromboxane and leukotriene syn- thesis by pyridoxine might be beneficial in disorders where the production of prostacyclin is decreased and the formation of thromboxane and cysteinyl leukotrienes is enhanced. Nicotinic acid and pyridoxine are B-complex vitamins. Nic- otinic acid, after conversion into either nicotinamide aden- ine dinucleotide or nicotinamide adenine dinucleotide phos- phate, has diverse actions in electron transfer reactions in the respiratory chain. As a drug, nicotinic acid (Niaspan A ,