THE BETA-ADRENERGIC SYSTEM OF NON-ALLERGIC PATIENTS WITH CHRONIC AIR-FLOW OBSTRUCTION AND EARLY MORNING DYSPNEA

: Lymphocyte beta-adrenergic receptor function and urinary excretion of catecholamines were measured in eight non-allergic patients with partially reversible chronic airflow obstruction (CAO) and early morning dyspnoea (EMD), and in eight matched healthy control subjects. In order to establish a possible relationship between the early morning dyspnoea and a reduced beta-adrenergic activity, these parameters were measured during the "morning dip" in FEV1 and in the afternoon, when lung function is maximal. No differences were observed for lymphocyte beta-adrenergic receptor characteristics (beta-receptor number, Kd, for 3H-dihydroalprenolol, and cAMP response to isoproterenol) between patients and controls, when determined at 8 AM or at 4 PM. Nor was there a significant circadian variation in these parameters present in both groups. By contrast, the patients showed a significantly reduced urinary excretion of epinephrine and norepinephrine, as measured in four-hourly urine portions collected between 8 and 12 AM and between 4 and 8 PM, respectively. In addition, the urinary excretion of epinephrine showed a significant circadian variation in the patients, which was correlated with the FEV1 (% predicted). Such a relationship was not found for norepinephrine. The results suggest that a (generalized) dysfunction of the beta-adrenergic receptor is not involved in the pathogenesis of CAO or EMD. However, reduced beta-adrenergic receptor stimulation due to decreased levels of catecholamines may contribute to the observed (variation in) airflow obstruction of the patients.