Background - The effects of beta(2) adrenergic agonists on chemorecept
ors remain controversial. This study was designed to examine whether f
enoterol, a beta(2) adrenergic agonist, increases the ventilatory resp
onses to hypercapnia (HCVR) and hypoxia (HVR) in normal subjects. Meth
ods - HCVR was tested with a rebreathing method and HVR was examined w
ith a progressive isocapnic hypoxic method in 11 normal subjects. Both
HCVR and HVR were assessed by the slope of occlusion pressure (P-0.1)
or ventilation (VE) plotted against end tidal carbon dioxide pressure
and arterial oxygen saturation, respectively. Respiratory muscle stre
ngth, spirometric values and lung volume were measured. After a single
oral administration of 5 mg fenoterol or placebo HCVR and HVR were ev
aluated. Results - Fenoterol treatment did not change the specific air
way conductance or forced expiratory volume in one second. Respiratory
muscle strength did not change. Fenoterol increased the slope of the
HCVR of both P-0.1 (from 0.251 (0.116) to 0.386 (0.206) kPa/kPa, avera
ge increase 71%) and Ve (from 10.7 (3.4) to 15.1 (4.2) 1/min/kPa, aver
age increase 52%), and shifted the response curves to higher values. F
or the HVR fenoterol increased the slopes of both P-0.1 and VE (from -
4.06 (2.00) x 10(-3) to -7.99 (4.29) x 10(-3) kPa/ %, an average incre
ase of 83%, and from -0.221 (0.070) to -0.313 (0.112) 1/min/%, a 44.5%
increase, respectively), and shifted the response curves to higher va
lues. Conclusion - Acute administration of fenoterol increases the ven
tilatory responses to both hypercapnia and hypoxia in normal subjects.