The effects of unloading the carotid sinus baroreceptors before and during the development of perinephritic hypertension were studied in conscious dogs instrumented with aortic catheters to measure arterial pressure and heart rate, and electromagnetic flow probes to measure cardiac output and calculate total peripheral resistance. Prior to hypertension, bilateral carotid occlusion (BCO) increased mean arterial pressure by 38 ± 2 from 101 ± 2 mm Hg and total peripheral resistance by 19 ± 2 from 46 ± 3 mm Hg/l/min, while cardiac output and heart rate did not change from 2,299 ± 128 ml/min and 84 ± 4 beats/min, respectively. At 2 weeks after renal wrapping, there were significant increases in baseline mean arterial pressure, cardiac output, and total peripheral resistance and decreases in heart rate; BCO increased mean arterial pressure by 59 ± 5 from 130 ± 4 mm Hg, heart rate by 36 ± 5 beats/min from 69 ± 3 beats/min, and cardiac output by 458 ± 103 from 2,711 ± 239 ml/min. By 4 weeks after renal wrapping, heart rate and mean arterial pressure responses to BCO were approaching baseline levels. After β-adrenergic receptor blockade, responses to BCO of mean arterial pressure, cardiac output, and heart rate were no longer significantly enhanced during the development of hypertension. Thus, in conscious dogs, reflex pressor responses to baroreceptor unloading via BCO were enhanced during the development of hypertension but no longer present 3 weeks later. The augmented mean arterial pressor responses to BCO were mediated by increases in cardiac output and heart rate, which in turn, appeared to be controlled by β-adrenergic receptor mechanisms. (Circulation Research 1987;61:678-686)