The objective of this study was to determine if ablation of the lateral parabrachial nucleus (
LPBN) would prevent
angiotensin II-induced
hypertension in rats. Thirteen male Sprague-Dawley rats were studied. Bilateral electrolytic lesions in the
LPBN were produced in six rats; the remaining seven rats were subjected to
sham lesion surgery only. All rats were instrumented with
vascular catheters and housed in metabolism cages. Daily measurements during the 16-day protocol included arterial pressure, heart rate, water intake, urine output, and urinary
sodium excretion. Periodically throughout the protocol depressor responses to
ganglion blockade and to blockade of V1-type
vasopressin receptors also were measured. The protocol was divided into three control-period days, 10 days of continuous (24 hr/day)
angiotensin II infusion (10 ng/min i.v.), and three recovery-period days. There were no significant differences between the two groups of rats for any variable during the control period. During
angiotensin II infusion,
sham-lesion rats exhibited a progressive increase in arterial pressure and the depressor response to
ganglion blockade and a decrease in urinary
sodium excretion. No other variable was significantly changed. In rats with
LPBN lesions, arterial pressure was significantly increased only on days 1 and 3 of
angiotensin II infusion. No other variable was affected. It was concluded that ablation of the
LPBN in rats prevented sustained
hypertension during
intravenous infusion of
angiotensin II by interfering with neurogenic pressor mechanisms normally activated by the
peptide.