Baroreflex mediated control of heart rate and vascular capacitance in trout

The baroreflex was triggered by altering branchial blood pressure with pre- and post-branchial occlusions for 30 s in rainbow trout Oncorhynchus mykiss. The cardiac limb of the baroreflex was monitored by continuous heart rate (f(H)) measurements. Responses of venous capacitance vessels were assessed, immediately following either occlusion, by measuring mean circulatory filling pressure (MCFP). Arterial responses were evaluated as the change in dorsal aortic blood pressure (P(da)) before and after pre-branchial occlusion. In untreated fish pre-branchial occlusion resulted in tachycardia (62.4+/-2.4 to 69.1+/-1.7 beats min(-1)), decreased venous capacitance reflected as an increase in MCFP (0.17+/-0.03 to 0.27+/-0.03 kPa) and increased P(da) (4.0+/-0.2 kPa compared to 3.2+/-0.1 kPa before occlusion). Post-branchial occlusion somewhat reversed the responses since f(H) decreased (62.4+/-2.4 to 53.0+/-3.1 beats min(-1)), whereas MCFP remained unaltered. Treatment with the alpha-adrenergic blocker prazosin (1 mg kg(-1)) increased resting MCFP to 0.33+/-0.03 kPa and appeared to abolish both venous and arterial responses to branchial occlusion. Subsequent atropine treatment (1.2 mg kg(-1)) abolished all chronotropic responses. We present for the first time ample evidence for baroreflex-mediated control of cardiovascular homeostasis, including both the chronotropic and the vascular limb of the baroreflex in an unanaesthetized fish. Furthermore, a novel technique to cannulate and occlude the dorsal aorta, using a Fogarty thru-lumen embolectomy catheter, is explained.