Q. Li et al., FOS-LIKE IMMUNOREACTIVITY IN THE MEDULLA AFTER ACUTE AND CHRONIC ANGIOTENSIN-II INFUSION, The Journal of pharmacology and experimental therapeutics, 284(3), 1998, pp. 1165-1173
Acute and chronic angiotensin (Ang) II hypertension are reported to ha
ve different mechanisms that involve differential contributions of the
peripheral vasculature and the nervous system. Acute Ang II hypertens
ion is mediated primarily by Ang acting at vascular smooth muscle, whe
reas chronic Ang II hypertension appears to have a neural component. I
n our experiments, the transition from a peripheral to a neural effect
occurs over 10 hr of Ang II infusion in rats. To identify the role of
the central nervous system in this transition, we measured Fos immuno
reactivity, an indicator of neural activity, in the nucleus of the sol
itary tract (NTS), caudal ventrolateral medulla (CVL) and rostral vent
rolateral medulla (RVL) in normal, sinoaortic denervated (SAD) and sha
m SAD rats after 2- or 18-hr Ang II infusion (50 ng/kg/min intravenous
ly). Vehicle (5% dextrose) was infused in normal rats as control. Comp
arable increases in arterial pressure were produced by 2- and 18-hr An
g II infusion in all groups. Fos was increased in the NTS in sham SAD
rats by 2- and 18-hr Ang II infusion (P < .05 vs. vehicle control). In
the CVL, only 2-hr Ang II infusion was associated with increased Fos
in normal and sham SAD rats (P < .05 vs. vehicle control) but not in S
AD rats. In the RVL, 18-hr Ang II infusion elevated Fos in all groups
(P < .05 vs. vehicle control). Activation of NTS during Ang II infusio
n is baroreceptor mediated and independent of infusion duration. Acute
Ang II infusion produced a baroreceptor-mediated activation of the CV
L, a region associated with baroreflex sympathoinhibition. Chronic Ang
II infusion produced a baroreceptor-independent activation of the RVL
, a brain area associated with sympathoexcitation, suggesting a centra
lly mediated increase in sympathetic outflow that may be associated wi
th chronically infused Ang II.