Plasma beta-endorphin and adenosine concentration in pulmonary hypertension

To determine whether β-endorphin plays a role in the regulation of pulmonary vascular tone in patients with pulmonary hypertension, we investigated the relations between hemodynamics and β-endorphin and adenosine concentrations in 3 clinical situations: (1) normal hemodynamics (7 subjects, mean pulmonary artery [PA] pressure 18.5 ± 1 mm Hg); (2) moderate pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD) (8 patients, mean PA pressure 31 ± 3 mm Hg); and (3) severe primary pulmonary hypertension (PPH) (8 patients, mean PA pressure 70 ± 5 mm Hg). Plasma β-endorphin and adenosine were measured in a distal PA and in the femoral artery in room air and during oxygen inhalation. Beta-endorphin levels were similar in the pulmonary and systemic circulations. No difference was observed between patients with COPD and PPH, but relative to controls, both had significantly higher β-endorphin levels. Pulmonary adenosine was significantly lower in patients with pulmonary hypertension than in controls (−60% in COPD [p <0.005] and −70% in PPH [p <0.001]). Pure oxygen administration significantly decreased adenosine and β-endorphin levels, much more so in patients with COPD and PPH. We found a negative correlation between β-endorphin and adenosine concentrations (r = −0.751, p <0.001): the higher the adenosine, the lower the β-endorphin level. These observations suggest that because adenosine release by pulmonary vascular endothelium is reduced in pulmonary hypertension, the resulting worsened hypoperfusion and tissue oxygenation may cause increased β-endorphin release.