Cardiovascular responses in the sea raven, Hemitripterus americanus, elicited by vascular compression.

Increases in the water pressure (PW) around the trunk of the sea raven (Hemitripterus americanus Gmelin) were used to evaluate the effects of vascular compression on cardiovascular variables. Cardiac output (Vb), heart rate (fH) and blood pressures in the ventral aorta, dorsal aorta and ductus Cuvier (Pva, Pda and Pdc, respectively) were measured. A 20 cm H2O increase in PW decreased vascular conductance by up to 25%. During vascular compression, a reflex bradycardia reduced Vb and attenuated the accompanying rise in arterial blood pressure. Pretreatment of the fish with the sympathetic antagonist, propranolol, further attenuated the hypertension by accentuating the reflex bradycardia. Subsequent pretreatment with papaverine, a vascular smooth muscle poison, potentiated these effects and did not reveal any autoregulatory vasodilation in the periphery. Atropine pretreatment completely abolished the reflex bradycardia, indicating that the bradycardia resulted from increased vagal cholinergic tone. The fish also exhibited cardiovascular compensation during the 2 min vascular compression. An accommodation of the barostatic reflex (reduced vagal tone) and a sympathetic tachycardia raised Vb and passively increased vascular conductance. The set point for the barostatic bradycardia was apparently temperature-sensitive.