To evaluate the effects of intravenously administered ritodrine hydrochloride on sodium and water metabolism, a pregnant baboon model was studied. Animals given ritodrine retained significantly more sodium (p < 0.001) and administered fluids (p < 0.002) compared with control animals. Although plasma volume did not change significantly within or between the two groups, extracellular volume increased by a mean of 1,480 ml in those given ritodrine compared with 790 ml in the control animals. There was no significant difference between animals given ritodrine and their controls regarding serial hematocrits, serum sodium, or colloid oncotic pressures. From this we conclude that the retained sodium and water was in the interstitial space. Since plasma volume was unaltered by ritodrine administration it seems unlikely that pure volume overload can explain the pulmonary edema induced by β-mimetics. Combined with the prior observation that direct pulmonary capillary membrane toxicity does not occur, the likely pathophysiology of β-agonist-induced pulmonary edema invclves left ventricular failure. © 1983.