The role of venous capacitance, circulating catecholamines, and heart rate in the hemodynamic response to increased temperature and hypoxia in the dogfish

Abstract

Hypoxia and increased temperature alter venous blood pressures in teleosts through active changes in venous tone. Elasmobranchs possess a capacious venous system but have limited adrenergic vascular innervation and subambient central venous pressure (Pcv). In this study, we explored venous hemodynamic responses to acute temperature increase and moderate (6.9 kPa) and severe (2.5 kPa) hypoxia in the dogfish ( Squalus acanthias). Normoxic dogfish at 10°C had a Pcvbetween −0.08 and −0.04 kPa and a mean circulatory filling pressure (Pmcf) of ∼0.12 kPa. At 16°C, heart rate ( fH), cardiac output (Q), and Pmcfincreased but Pcvand plasma epinephrine and norepinephrine levels were unchanged. In contrast, moderate and severe hypoxia increased Pcvand decreased Q and stroke volume (VS). fHdecreased in severe hypoxia, whereas Pmcfwas unaffected despite elevated catecholamine levels. Atropine abolished hypoxic reductions in Q, VS, and fH, but Pcvstill increased. In contrast to the response in teleosts, this study on dogfish suggests that venous capacitance changes associated with warming and hypoxia are minimal and likely not mediated by circulating catecholamines. Thus hemodynamic status of the capacious elasmobranch venous circulation is potentially regulated by blood volume shifts from passive flow-mediated events and possibly through myogenic mechanisms.