Sub-ambient central venous pressure (P_ven) and modulation of venous return through cardiac suction (vis a fronte) characterizes the venous circulation in sharks. Venous function was estimated in dogfish, Squalus acanthias, by measuring the mean circulatory filling pressure (MCFP) during transient occlusion of cardiac outflow. We tested the hypothesis that venous return and cardiac preload can be altered additionally through adrenergic activation. The experiments involved surgical opening of the pericardium to place a perivascular occluder around the conus arteriosus. Another control group was identically instrumented, but lacking the occluder, and subjected to the same pharmacological protocol to evaluate how pericardioectomy affected cardiovascular status. Routine Pven was negative (-0.08±0.02 kPa) in control fish, but positive (0.09±0.01 kPa) in the pericardioectomized group. Injections of 5 µg kg body mass^-1 (Mb) of adrenaline and phenylephrine (100 µg kg Mb^-1) increased P_ven and MCFP, whereas isoproterenol (1 µg kg Mb^-1) decreased both variables. Thus, constriction and relaxation of the venous vasculature were mediated through the respective stimulation of - and -adrenergic receptors. -Adrenergic blockade with prazosin (1 mg kg Mb^-1) attenuated the responses to phenylephrine and decreased resting P_ven in pericardioectomized animals. Our results provide convincing evidence for adrenergic control of the venous vasculature in elasmobranchs, although the pericardium is clearly an important component in the modulation of venous function. Thus, active changes in venous capacitance have previously been underestimated as an important means of modulating venous return and cardiac performance in this group.