The purpose of this study was to determine whether sinoaortic deafferentati
on (SAD) alters the severity of hypertension or sympathoadrenal contributio
n to mean blood pressure (MAP) during renal wrap hypertension. Male Sprague
-Dawley rats were implanted with radiotelemetry transmitters for 24-hour re
cording of MAP and heart rate. All rats underwent either SAD or sham SAD (I
ntact) 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) grou
p in which 1-kidney figure-8 renal wrap was performed. SAD increased the ac
ute MAP response to renal wrap (Intact-Sham=5+/-1 mmHg, Intact-Wrap=45+/-3
mm Hg, SAD-Sham=3+/-3 mm Hg, SAD-Wrap=58+/-4 mm Hg) and increased the labil
ity of MAP (SD of MAP; Intact-Sham=3.8+/-0.2, Intact-Wrap=4.2+/-0.3, SAD-Sh
am=9.6+/-1.4, SAD-Wrap=9.7+/-1.4), MAP was not different between SAD and In
tact rats during 4 weeks after renal wrap or sham surgery; however, inducti
on of hypertension produced additional MAP variability that was independent
of SAD (Intact-Shaln=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 con
tribution to MAP was assessed by the depressor response to ganglionic block
ade and plasma norepinephrine at rest and after neuronal uptake inhibition
with desipramine, The depressor response to ganglionic blockade was signifi
cantly increased by renal wrap and by SAD (Intact-Sham=-49+/-2 mm Hg, Intac
t-Wrap=-73+/-4 mm Hg, SAD-Sham=-77+/-5 mm Hg, SAD-Wrap=-96+/-6 mm Hg). In t
he 3 groups with enhanced ganglionic blockade responses, desipramine caused
a significant increase in plasma norepinephrine. These results indicate th
at SAD does not alter the development of renal wrap hypertension but does i
ncrease the sympathoadrenal contribution to MAP in both normotensive and hy
pertensive animals.