Centrally administered Angiotensin II acting on brain AT1 receptors significantly induced adrenaline secretion from the adrenal medulla and pressor responses in male rats.
Central administration of Angiotensin II activates brain AT1 receptors to selectively induce adrenal adrenaline secretion and pressor responses, highlighting a central mechanism for blood pressure modulation.
p-value: p=<0.05
Angiotensin II (AngII) plays important roles in the regulation of cardiovascular function. Both peripheral and central actions of AngII are involved in this regulation, but mechanisms of the latter actions as a neurotransmitter/neuromodulator within the brain are still unclear. Here we show that (1) intracerebroventricularly (i.c.v.) administered AngII in urethane-anesthetized male rats elevates plasma adrenaline derived from the adrenal medulla but not noradrenaline with valsartan- (AT1 receptor blocker) sensitive brain mechanisms, (2) peripheral AT1 receptors are not involved in the AngII-induced elevation of plasma adrenaline, although AngII induces both noradrenaline and adrenaline secretion from bovine adrenal medulla cells, and (3) i.c.v. administered AngII elevates blood pressure but not heart rate with the valsartan-sensitive mechanisms. From these results, i.c.v. administered AngII acts on brain AT1 receptors, thereby inducing the secretion of adrenaline and pressor responses. We propose that the central angiotensinergic system can activate central adrenomedullary outflow and modulate blood pressure.
Nakamura et al. (Fri,) conducted a other in Healthy (animal model) (n=60). Intracerebroventricular Angiotensin II vs. Vehicle (saline) was evaluated on Plasma adrenaline levels and blood pressure (p=<0.05). Centrally administered Angiotensin II acting on brain AT1 receptors significantly induced adrenaline secretion from the adrenal medulla and pressor responses in male rats.