In experiments on isolated rat uteri the relation was studied between the mechanical effects of catecholamines and the level of adenosine 3′,5′-monophosphate (cAMP). Adrenaline (1–100 ng/ml) caused relaxation of isolated rat uteri and a highly significant increase in the tissue cAMP concentration; both relaxation and cAMP increase were blocked by propranolol or butoxamine but unaffected by phenoxybenzamine. The rise in cAMP level was maintained in a Ca-free solution when the muscle could not contract. The stimulation of α-receptors of propranolol-pretreated uteri induced contractions but it caused no change in the cAMP concentration. cAMP level, increased by a previous application of isoproterenol, remained unchanged when the uterus contracted after application of oxytocin, propranolol, or propranolol with adrenaline. cAMP levels remained elevated after previous adrenaline whether oxytocin dose–effect curves were still shifted to the right or were shifted back by subsequent propranolol. Adrenaline decreased significantly the ATP concentration in the uterus. The effect persisted with a propranolol blockade but was reversed to an increase by pretreatment with phenoxybenzamine or in a Ca-free solution. We conclude that the level of cAMP in the uterus is controlled by mechanisms related to β-receptors but that α-receptor mechanisms do not affect cAMP levels. Also the level of cAMP is not the primary determinant of uterine motility.