Effect of β2-adrenergic receptor functioning and increased norepinephrine on the hypercoagulable state with mental stress

Background Procoagulant stress responses may contribute to atherosclerosis development and acute coronary thrombosis. In the present study, we examined the role of beta(2)-adrenergic receptor function and plasma catecholamines in the stress-induced increase in the 2 hypercoagulability markers thrombin-antithrombin III (TAT) complex and fibrin D-dimer (DID). Methods Lymphocyte beta(2)-adrenoreceptor sensitivity and density were assessed at rest, and plasma levels of TAT, DID, epinephrine, and norepinephrine were measured at rest and in response to a standardized mental stress task in 19 normotensive and mildly hypertensive nonmedicated subjects (mean age 38 years, age range 29 to 48 years). Results The stressor elicited a significant increase in TAT (P =.024), DID (P =.026), and norepinephrine (P =.005). Resting beta(2)-adrenoreceptor sensitivity (isoproterenol-stimulated cyclic adenosine monophosphate production) plus the norepinephrine change scores (stress minus rest) accounted for 59% of the variance in the absolute TAT increase in response to stress (P =.001). Hypertension status and demographic variables such as sex did not influence the results. Conclusions Acute mental stress may trigger a hypercoagulable state evidenced by increased thrombin activity and increased fibrin turnover. beta(2)-Adrenergic receptor sensitivity and plasma catecholamine activity may mediate the procoagulant response to acute stressors. These mechanisms may help explain the adverse impact of mental stress on the cardiovascular system.