The platelet α2-adrenoceptor and prostacyclin sensitivity are not altered by cigarette smoking — A study of monozygotic twin pairs discordant for smoking

Abstract

A study with ten identical twin pairs discordant for cigarette smoking for over 20 years was undertaken to evaluate the effect of smoking on platelet α2-adrenoceptor binding ([ 3H]-yohimbine) and prostacyclin (Iloprost R) sensitivity. Since plasma catecholamines, adrenaline and noradrenaline were increased in smokers (3.95 ± 0.7 vs 2.26 ± 0.1 pmol/ml, p <0.05) at rest, the objective of an acute additional adrenergic discharge by physical exercise was to uncover possible tachyphylaxis. Aggregation of adrenaline-stimulated platelets was significantly reduced in smokers after exercise and the refractoriness appeared to be maintained for 15 and 30 min afterwards. However, the densities of binding sites for the radioligand were not markedly different between the study groups at rest or after exercise. The binding affinity decreased after exercise in both groups. Adrenaline-stimulated platelets responded to prostacyclin by inhibiting aggregation and activating cAMP production equally in smokers and nonsmokers implying a preserved sensitivity to prostacyclin. Although smoking introduces long-term sympathoadrenergic effects, it does not alter α2-adrenoceptor binding in platelets. Thus, the present data support a theory that smoking mediates its effects by platelet to vessel wall interaction and vasoactivity, rather than directly changing the properties of adrenoceptor in platelet or the coupling to adenylate cyclase.