CIGARETTE SMOKING INHIBITS PROSTACYCLIN FORMATION

Abstract

Urinary prostacyclin (PGI 2) 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 PGI 2, was given to smokers and non-smokers. PGI 2 was measured as the stable metabolite, 6-keto-PGF 1α in 4 h urine samples by radioimmunoassay after chromatography on LH-20 'Sephadex'. Smoking of nicotine-free cigarettes had no effect on PGI 2 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-PGF 1α. In contrast, when chronic smokers used nicotine-containing cigarettes there was a highly significant reduction in excretion of 6-keto-PGF 1α (192±20 to 138±17 ng/g creatinine). Noradrenaline increased PGI 2 in non-smokers (181±16 to 348±56) but not in smokers. Smoking of nicotine-containing tobacco abolished the PGI 2 response to noradrenaline. These observations suggest that inhalation of nicotine-containing tobacco smoke reduces vascular PGI 2 production; this may be a factor in the development of accelerated cardiovascular disease.