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 (P(ET)CO2) have been defined in 10 anesthetized, intubated rhesus monkeys (mean age 7.0 y, weight 10.2 kg). VO2 increased 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. P(ET)CO2 dropped dramatically after theophylline (-15.7%, p < 0.001), but not at all with any of the inhaled beta2-adrenoceptor agonists. In seven animals, salbutamol (albuterol) caused an increase in V(E) and VO2 of 50.1% and 45.9%, respectively, whereas in the presence of a beta2-adrenoceptor antagonist [racemic or (+/-)-propranolol (0.1 mg/kg i.v.)], inhaled salbutamol (2.5 mg/mL for 10 min) could not increase V(E) (+6.2%, p > 0.05) and VO2 (+1.6%, p > 0.05). The increase in VO2 and V(E) after administration of beta2-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 VO2 and V(E) after salbutamol was suppressed in the presence of propranolol, which is consistent with a beta-receptor-mediated mechanism.