Cigarette smoking inhibits prostacyclin formation.

Urinary prostacyclin (PGI2) was measured in 12 chronic smokers and 12 non-smokers after inhalation of smoke from nicotine-containing and nicotine-free cigarettes. In a separate study a pressor dose of noradrenaline, which increases PGI2, was given to smokers and non-smokers. PGI2 was measured as the stable metabolite, 6-keto-PGF1 alpha in 4 h urine samples by radioimmunoassay after chromatography on LH-20 'Sephadex'. Smoking of nicotine-free cigarettes had no effect on PGI2 release in either smokers or non-smokers. In non-smokers inhalation of nicotine-containing tobacco smoke increased heart-rate, blood-pressure, and urine osmolality, but did not affect urinary 6-keto-PGF1 alpha. In contrast, when chronic smokers used nicotine-containing cigarettes there was a highly significant reduction in excretion of 6-keto-PGF1 alpha (192 +/- 20 to 138 +/- 17 ng/g creatinine). Noradrenaline increased PGI2 in non-smokers (181 +/- 16 to 348 +/- 56) but not in smokers. Smoking of nicotine-containing tobacco abolished the PGI2 response to noradrenaline. These observations suggest that inhalation of nicotine-containing tobacco smoke reduces vascular PGI2 production; this may be a factor in the development of accelerated cardiovascular disease.