In human heart there is now evidence for the involvement of four β-adrenoceptor populations, three identical to the recombinant β₁-, b₂- and β₃-adrenoceptors, and a fourth as yet uncloned putative β-adrenoceptor population, which we designate provisionally as the cardiac putative β₄-adrenoceptor. This review described novel features of β-adrenoceptors as modulators of cardiac systolic and diastolic function. We also discuss evidence for modulation by unoccupied β₁- and β₂-adrenoceptors. Human cardiac and recombinant β₁- and β₂-adrenoceptors are both mainly coupled to adenylyl cyclase through Gs protein, the latter more tightly than the former. Activation of both human β₁- and β₂-adrenoceptors not only increases cardiac force during systole but also hastens relaxation through cyclic AMP-dependent phosphorylation of phospholamban and troponin I, thereby facilitating diastolic function. Furthermore, both β₁ and β₂-adrenoceptors can mediate experimental arrhythmias in human cardiac preparations elicited by noradrenaline and adrenaline. Human ventricular β₃-adrenoceptors appear to be coupled to a pertussis toxin-sensitive protein (Gi?). β₃-Adrenoceptor-selective agonists shorten the action potential and cause cardiodepression, suggesting direct coupling of a Gi protein to a K⁺ channel. In a variety of species, including man, cardiac putative β₄-adrenoceptors mediate cardiostimulant effects of non-conventional partial agonists, i.e. high affinity β₁- and β₂-adrenoceptor blockers that cause agonist effects at concentrations considerably higher than those that block these receptors. Putative β₄-adrenoceptors appear to be coupled positively to a cyclic AMP-dependent cascade and can undergo some desensitisation.