The purpose of this study was to determine whether sinoaortic deafferentation (SAD) alters the severity of hypertension or sympathoadrenal contribution to mean blood pressure (MAP) during renal wrap hypertension. Male Sprague-Dawley rats were implanted with radiotelemetry transmitters for 24-hour recording of MAP and heart rate. All rats underwent either SAD or sham SAD (Intact) surgery and were allowed to recover for 10 to 14 days. The rats were then assigned to a normotensive (Sham) group or a hypertensive (Wrap) group in which 1-kidney figure-8 renal wrap was performed. SAD increased the acute MAP response to renal wrap (Intact-Sham=5+/-1 mm Hg, Intact-Wrap=45+/-3 mm Hg, SAD-Sham=3+/-3 mm Hg, SAD-Wrap=58+/-4 mm Hg) and increased the lability of MAP (SD of MAP; Intact-Sham=3.8+/-0.2, Intact-Wrap=4.2+/-0.3, SAD-Sham=9. 6+/-1.4, SAD-Wrap=9.7+/-1.4). MAP was not different between SAD and Intact rats during 4 weeks after renal wrap or sham surgery; however, induction of hypertension produced additional MAP variability that was independent of SAD (Intact-Sham=4.6+/-0.4, Intact-Wrap=6.2+/-0.6, SAD-Sham=6.3+/-0.5, SAD-Wrap=10.8+/-1.5). In a separate group of rats, the sympathoadrenal contribution to MAP was assessed by the depressor response to ganglionic blockade and plasma norepinephrine at rest and after neuronal uptake inhibition with desipramine. The depressor response to ganglionic blockade was significantly increased by renal wrap and by SAD (Intact-Sham=-49+/-2 mm Hg, Intact-Wrap=-73+/-4 mm Hg, SAD-Sham=-77+/-5 mm Hg, SAD-Wrap=-96+/-6 mm Hg). In the 3 groups with enhanced ganglionic blockade responses, desipramine caused a significant increase in plasma norepinephrine. These results indicate that SAD does not alter the development of renal wrap hypertension but does increase the sympathoadrenal contribution to MAP in both normotensive and hypertensive animals.