Background
Resistive breathing (RB) due to airflow limitation is the pathophysiologic hallmark of chronic obstructive pulmonary disease (COPD). Nitric oxide (NO) is a physiological regulator of smooth muscle tone that acts through activation of soluble guanylyl cyclase (sGC). We hypothesized that increased smooth muscle tone limiting airflow in COPD could result from reduced sGC. Herein, we investigated the expression and downstream signalling of sGC in RB.