Previous findings suggest that chronic ANG II-induced hypertension is neurally mediated while acute ANG II hypertension results from direct action on the vasculature. In our hands, transition from a peripheral to a neural effect occurs over about 10 h of ANG II infusion in rats. To identify the role of medullary areas involved in blood pressure control in this transition, we measured Fos, as an indication of neural activity, in the nucleus tractus solitarus (NTS), caudal ventrolateral medulla (CVL) and rostral ventrolateral medulla (RVL) in intact, sham and SAD rats after 2 or 18 h ANG II (50 ng/kg/min, i.v.) infusion. Comparable increases in arterial pressure were produced by ANG II infusion in all groups. In the NTS, Fos was increased by 2 and 18 h ANG II infusion in normal and sham rats (n=4 for each group, P<0.05 vs intact vehicle control). These increases were not observed in SAD rats (n=4). In the CVL, only 2 h ANG II infusion was associated with increased Fos in normal and sham rats (P<0.05 vs intact vehicle control). This increase in the CVL was not observed in SAD rats. In the RVL, 18 h but not 2 h ANG II infusion elevated Fos in all groups (P<0.05 vs intact vehicle control). These data suggest that activation of NTS during ANG II infusion is baroreflex-mediated and independent of infusion time. Acute ANG II infusion produced a baroreflex-mediated activation of the CVL, a region associated with baroreflex sympathoinhibition. Chronic ANG II infusion produced a baroreceptor-independent activation of the RVL, a brain area containing bulbospinal neurons and associated with sympathoexcitation. Thus, SAD prevented increases in Fos in the NTS and CVL produced by ANG II infusion but failed to influence Fos produced in the RVL by ANG II Infusion.
|State||Published - 1 Dec 1997|