Inhaled β-agonist does not modify sympathetic activity in patients with COPD

Background Neurohumoral activation is present in patients with COPD and might provide a link between COPD and systemic effects, especially cardiovascular disease. We aimed to evaluate if inhaled therapy with the long-acting β-agonist (LABA) bronchodilator salmeterol modifies muscle sympathetic nerve activity (MSNA) as evaluated by microneurography. Methods MSNA, heart rate, blood pressure, and respiration were continually measured as placebo and salmeterol were administered sequentially. The primary endpoint was the acute effect of salmeterol on MSNA/100 heart beats. Additionally, plasma catecholamine levels and arterial pulse wave velocity were evaluated. Following 4 weeks of treatment with salmeterol 50 µg twice daily, measurements were repeated without placebo administration. Results A total of 32 COPD patients were included. A valid MSNA signal for the primary endpoint was derived from 18 patients. After acute administration of salmeterol there was no significant change in MSNA/100 heart beats vs. placebo [72.96 ± 14.716 (SD) vs. 73.30 ± 10.767; p=0.5062]. Likewise, no changes in MSNA from baseline were observed after 4 weeks of salmeterol treatment. MSNA was positively correlated with plasma norepinephrine levels. Heart rate slightly increased as an acute and long-term effect, while blood pressure and arterial pulse wave velocity were unchanged. Treatment with salmeterol was safe and well tolerated. Conclusion By using microneurography as a gold standard to evaluate sympathetic activity we found no change in MSNA following salmeterol inhalation. Thus a negative effect of β-agonists on sympathetic activation cannot be inferred by these data.