Carotid baroreflex pressor responses at rest and during exercise: cardiac output vs. regional vasoconstriction

The arterial baroreflex mediates changes in arterial pressure via reflex ch anges in cardiac output (CO) and regional vascular conductance, and the rel ative roles may change between rest and exercise and across workloads. Ther efore, we quantified the contribution of CO and regional vascular conductan ces to carotid baroreflex-mediated increases in mean arterial pressure (MAP ) at rest and during mild to heavy treadmill exercise (3.2 kph; 6.4 kph, 10 % grade; and 8 kph, 15% grade). Dogs (n = 8) were chronically instrumented to measure changes in MAP, CO, hindlimb vascular conductance, and renal vas cular conductance in response to bilateral carotid occlusion (BCO). At rest and at each workload, BCO caused similar increases in MAP (average 35 +/- 2 mmHg). In response to BCO, neither at rest nor at any workload were there significant increases in CO; therefore, the pressor response occurred via peripheral vasoconstriction. At rest, 10.7 +/- 1.4% of the rise in MAP was due to vasoconstriction in the hindlimb, whereas 4.0 +/- 0.7% was due to re nal vasoconstriction. Linear regression analysis revealed that, with increa sing workloads, relative contributions of the hindlimb increased and those of the kidney decreased. At the highest workload, the decrease in hindlimb vascular conductance contributed 24.3 +/- 3.4% to the pressor response, whe reas the renal contribution decreased to only 1.6 +/- 0.3%. We conclude tha t the pressor response during BCO was mediated solely by peripheral vasocon striction. As workload increases, a progressively larger fraction of the pr essor response is mediated via vasoconstriction in active skeletal muscle a nd the contribution of vasoconstriction in inactive beds (e.g., renal) beco mes progressively smaller.