Central venous blood pressure (P_ven) increases in response to hypoxia in rainbow trout (Oncorhynchus mykiss), details on the control mechanisms of the venous vasculature during hypoxia are unstudied in fish. Basic cardiovascular variables including P_ven, dorsal aortic blood pressure (P_da), cardiac output (Q) and heart rate (f_H) were monitored in vivo during normoxia and moderate hypoxia (P_WO₂= ~9 kPa). Venous capacitance curves for normoxia and hypoxia were constructed at 80-100%, 90-110% and 100-120% of total blood volume by transiently (8 s) occluding the ventral aorta to measure P_ven during circulatory arrest and estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance (C). MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by -adrenoceptor blockade with prazosin (1 mg kg-1 Mb). MCFP still increased during hypoxia after pre-treatment with the adrenergic nerve-blocking agent bretylium (10 mg kg^-1 M_b), but the decrease in USBV only persisted at 80-100% blood volume whereas C decreased significantly at 90-110% blood volume. In all treatments, hypoxia typically reduced fH while Q was maintained with compensatory increase in stroke volume (SV). Despite the markedly reduced response in venous capacitance after adrenergic blockade, P_ven always increased in response to hypoxia. This study reveals for the first time that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an -adrenergic mechanism with both humoral and neural components.