Vl. Brooks et Dc. Hatton, CHRONIC ANG-II INFUSION AND REFLEX CONTROL OF NOREPINEPHRINE AND CORTICOSTERONE IN CONSCIOUS RABBITS, American journal of physiology. Regulatory, integrative and comparative physiology, 41(2), 1997, pp. 487-496
The hypothesis that long-term increases in angiotensin II (ANG II) pro
duce pressure-independent resetting of baroreflex control of the sympa
thetic nervous system and the hypothalamic-pituitary-adrenal axis was
tested in rabbits by determining the effect of chronic ANG II infusion
on reflex relationships between mean arterial pressure (MAP) and plas
ma concentrations of norepinephrine (NE) and corticosterone (CS). Afte
r 2 wk, ANG II increased MAP from 61 +/- 1 to 99 +/- 2 mmHg (P < 0.05)
without altering heart rate or plasma NE concentration, but increased
CS from 9.8 +/- 1.3 to 29.5 +/- 13.7 ng/ml (P < 0.05). Heart rate, NE
, and CS baroreflex curves were all reset to a higher pressure level (
P < 0.05) after 24 h, 1 wk, and 2 wk of ANG II. Forty minutes after st
opping ANG II on the same days, MAP decreased, and curves were shifted
back toward control (P < 0.05), indicating that ANG II was required f
or the resetting. Two findings suggest that the resetting action of AN
G II is distinct from the presser effect. First, although stopping ANG
II reversed the hypertension as it reversed the resetting, reversal o
f the hypertension instead by prolonged infusion of nitroprusside alon
g with ANG II did not have the same effect. Second, NE and heart rate
baroreflex curves returned toward preinfusion positions after stopping
ANG II (P < 0.05), even when the hypertension was nearly maintained b
y phenylephrine infusion. In conclusion, chronic increases in ANG II m
ay have a global baroreflex resetting effect by a mechanism that is in
part independent of the hypertension.