Brain angiotensin (AngII) is an important neuromodulator of cardiovascular responses
induced by stress in several brain regions. The catecholaminergic A1 neurones of the
caudal ventrolateral medulla (CVLM), which is important for autonomic regulation,
is rich in AT1A receptors. We therefore examined whether the expression of AT1A receptors in the A1 cells of AT1A−/− mice alters baroreflex sensitivity and cardiovascular responses to stress. Bilateral
microinjections of lentivirus with the catecholamine-selective PRSx8 promoter driving
expression of either green fluorescent protein (GFPv) or AT1A receptors (AT1v mice) were made into the CVLM of AT1A−/− mice. Telemetry devices were used to record mean arterial pressure (MAP), heart rate
(HR) and locomotor activity. No differences in MAP or HR were recorded 5 weeks following lentivirus microinjection. However, baroreflex sensitivity was reduced
by 25% in AT1v mice (P<0.003). Cage-switch stress for one hour induced greater activation of forebrain and
hypothalamic neurons but 35% smaller MAP responses in AT1v mice compared with GFPv
mice (P<0.001). Reduced MAP mid frequency power reflected attenuated sympathetic activation
(Pgroup x stress=0.04). The reduction in cardiac baroreflex sensitivity during the one-hour aversive
stimulus was similar in both groups. These results suggest that AT1A receptors in noradrenergic A1 neurons of the CVLM do not contribute to basal BP or
HR but they normally inhibit cardiac vagal baroreflex activity. However, during an
activated state AT1A receptors in the CVLM amplify forebrain regions involved in emotional and autonomic
processing during stress resulting in increased locomotor activity. This is accompanied
by lesser increase in blood pressure due to sympatho-inhibitory influences possibly
directed to muscle dilatation to promote flight. Thus AT1A receptors on A1 neurons appear to provide a major advantage in adaptation to aversive
situations.
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© 2010 Published by Elsevier Inc.