Angiotensin type 1A receptors transfected into the A1 neurons inhibit baroreflex gain and the cardiovascular response to stress in AT 1A−/− mice

Abstract

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.