Unlike β1/β2AR, which are known to be downregulated and desensitized under sustained catecholamine stimulation, β3-AR expression was shown to be upregulated in the myocardium of heart failure (HF) patients [15], but also in animals models of HF [16,17], supporting less propensity for desensitization (see part 3 below). Here, ADRB3 is linked to hydrops fetalis.