The purpose of this study was to test the hypothesis that arbutamine, a specific B₁-adrenergic agonist, will not cause different circulatory and physiologic effects than the less specific endogenous catecholamines released in response to an exercise stress test in persons with known or suspected coronary artery disease. Nine male subjects, mean age 66 years, completed symptom-limited arbutamine (ESA) and exercise (ETT) stress tests in a randomized cross-over study. The ESA delivery device controlled infusion rate to induce a graded heart rate increase of 8 bt min⁻¹. Heart rate, systolic blood pressure, diastolic blood pressure, rate pressure product, ST segment shift, and specimens for epinephrine, norepinephrine, dopamine, cortisol, insulin, glucagon, glucose, free fatty acids, glycerol, and lactate were collected at baseline, immediate post-stress, and 10, 30, and 60 minutes post-stress. The research hypothesis was rejected. Repeated measures analysis of variance for each measure demonstrated a significant (p ≤ .05) time treatment interaction in heart rate, systolic blood pressure, rate pressure product, insulin, glucagon, glycerol, free fatty acid, and lactate responses and a significant time effect for cortisol response. Circulatory differences included higher systolic blood pressure and rate pressure product responses for ETT than ESA and a more rapid recovery of circulatory variables following ETT. Metabolic differences were due to higher free fatty acid and glycerol responses for ESA than ETT and a slower recovery of these metabolites and lactate following ESA. Hormonal differences included an earlier and greater magnitude rise in insulin response for ESA than ETT. There were no differences (p ≤ .05) by treatment, time, or time treatment interaction for diastolic blood pressure, ST segment shift, catecholamines, or glucose. In conclusion, arbutamine caused different circulatory and physiologic effects consistent with differences in adrenergic receptor activity. Arbutamine caused substantial B₁₊₂ agonist effects on hormonal and metabolic responses in cardiotonic doses employed clinically for diagnostic stress testing and may impact clinical interpretation of stress test results.