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Cigarette smoking inhibits prostacyclin formation.

J L Nadler, J S Velasco, R Horton

Lancet (London, England)

|June 4, 1983

Summary

Nicotine-containing cigarette smoke significantly reduces prostacyclin (PGI2) production in chronic smokers, unlike nicotine-free smoke. This reduction may contribute to cardiovascular disease development.

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Area of Science:

Cardiovascular Physiology
Pharmacology
Environmental Health

Background:

Prostacyclin (PGI2) is a vasodilator and inhibitor of platelet aggregation.
Cardiovascular disease is a leading cause of mortality, and smoking is a major risk factor.
The specific mechanisms by which smoking affects PGI2 production are not fully understood.

Purpose of the Study:

To investigate the effect of nicotine-containing and nicotine-free cigarette smoke on urinary prostacyclin (PGI2) levels in smokers and non-smokers.
To determine if nicotine-containing smoke alters the PGI2 response to noradrenaline, a known PGI2 stimulant.

Main Methods:

Urinary 6-keto-PGF1 alpha (a stable PGI2 metabolite) was measured by radioimmunoassay in 12 chronic smokers and 12 non-smokers.
Participants inhaled smoke from nicotine-containing and nicotine-free cigarettes.
A pressor dose of noradrenaline was administered to assess PGI2 response in a separate study.

Main Results:

Nicotine-free cigarettes had no effect on PGI2 levels in either group.
Nicotine-containing smoke inhalation did not affect PGI2 in non-smokers but significantly reduced it in chronic smokers.
Noradrenaline increased PGI2 in non-smokers, but this effect was abolished in smokers who inhaled nicotine-containing smoke.

Conclusions:

Inhalation of nicotine-containing tobacco smoke reduces vascular PGI2 production in chronic smokers.
This reduction in PGI2 may be a contributing factor to the accelerated cardiovascular disease observed in smokers.
Nicotine appears to be the component responsible for inhibiting PGI2 production and response.

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