The effects of breathing normal saline, salmeterol, fenoterol, ipratropium bromide, or formoterol, and of i.v. infusion of theophylline on oxygen consumption (˙Vo2), carbon dioxide production (˙Vco2), minute ventilation (˙Ve), heart and respiratory rates, and end-tidal carbon dioxide tension (PETco2) have been defined in 10 anesthetized, intubated rhesus monkeys (mean age 7.0 y, weight 10.2 kg).˙Vo2increased over control by +17.1% after salmeterol (p< 0.001), +33.3% after fenoterol (p< 0.001), +23.7% after formoterol (p< 0.001), +3.9% after theophylline (p< 0.01), but did not change after ipratropium bromide and normal saline. Ve increased by 63.0% after fenoterol (p< 0.001), 49.8% after formoterol (p< 0.001), 31.7% after salmeterol (p< 0.01), and 29.7% after theophylline (p< 0.001), but not after ipratropium bromide or normal saline. Heart rate response was greatest after fenoterol, formoterol, and salmeterol, respectively. PETco2dropped dramatically after theophylline (-15.7%,p< 0.001), but not at all with any of the inhaled β2-adrenoceptor agonists. In seven animals, salbutamol (albuterol) caused an increase in ˙Ve and˙Vo2of 50.1% and 45.9%, respectively, whereas in the presence of aβ2-adrenoceptor antagonist {racemic or (+/-)-propranolol (0.1 mg/kg i.v.)}, inhaled salbutamol (2.5 mg/mL for 10 min) could not increase˙Ve (+6.2%,p> 0.05) and ˙Vo2(+1.6%,p> 0.05). The increase in ˙Vo2and ˙Ve after administration of β2-agonists may be partly the result of direct stimulation of the respiratory center and partly a response to increased metabolic rate. The dramatic increase in ˙Vo2and ˙Ve after salbutamol was suppressed in the presence of propranolol, which is consistent with aβ-receptor-mediated mechanism.Abbreviations: PETco2, end-tidal carbon dioxide tension;Vco2, carbon dioxide production;˙Ve,minute ventilation;˙Vo2, total body oxygen consumption;˙Vo2resp, oxygen cost of breathing;Sao2, arterial oxygen saturation