The pericardial and peritoneal spaces of elasmobranch fishes are connected by the pericardioperitoneal canal (PPC), which allows pericardial fluid to escape when pressures exceed 0.1–0.3 kPA. Using the horn shark (Heterodontus francisci), we tested the hypothesis that the PPC functions to increase cardiac stroke volume by lowering pericardial pressure during activity. We also assessed the role of the PPC during coughing, feeding, or burst swimming and examined the effects of PPC occlusion. Increases in heart size were not prevented following augmented venous return in sharks with undisturbed or occluded PCP, evidence that argues that pericardial fluid loss through the PPC is a cause of increased cardiac stroke volume and not the result. Coughs, feeding, and burst swimming led to discharge of pericardial fluid. Chronic PPC occlusion resulted in an increased pericardial pressure, fluid volume, and frequency of coughing, and a decreased survival time compared to shams. Thus, in the horn shark the PPC likely compensates for constraints that may be imposed by the pericardium, provides a route for pericardial drainage, and regulates cardiac stroke volume during periods of activity.