Limits...
Angiotensin II acting on brain AT 1 receptors induces adrenaline secretion and pressor responses in the rat

View Article: PubMed Central - PubMed

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

Effects of valsartan and PD123319 on the centrally administered AngII-induced elevation of plasma adrenaline levels.Valsartan (Val) (AT1 receptor blocker) (100 nmol per animal), vehicle-1 (3 μl DMF per animal), PD123319 (PD) (AT2 receptor blocker) (100 nmol per animal), or vehicle-2 (5 μl saline per animal) was i.c.v. administered 30 min before the administration of AngII (3 nmol per animal, i.c.v.). (a and c) Increment of plasma adrenaline above the basal level. Arrows indicate the administration of Val (a)/PD (c)/vehicle-1/vehicle-2 and AngII. (b and d) AUC of the elevation of plasma adrenaline above the basal level for each group of (a) and (c), respectively. *P < 0.05, when compared to the vehicle-1- and AngII-treated group with an unpaired Student's t-test. The other conditions are the same as those of Figures 1 and 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC5384216&req=5

f3: Effects of valsartan and PD123319 on the centrally administered AngII-induced elevation of plasma adrenaline levels.Valsartan (Val) (AT1 receptor blocker) (100 nmol per animal), vehicle-1 (3 μl DMF per animal), PD123319 (PD) (AT2 receptor blocker) (100 nmol per animal), or vehicle-2 (5 μl saline per animal) was i.c.v. administered 30 min before the administration of AngII (3 nmol per animal, i.c.v.). (a and c) Increment of plasma adrenaline above the basal level. Arrows indicate the administration of Val (a)/PD (c)/vehicle-1/vehicle-2 and AngII. (b and d) AUC of the elevation of plasma adrenaline above the basal level for each group of (a) and (c), respectively. *P < 0.05, when compared to the vehicle-1- and AngII-treated group with an unpaired Student's t-test. The other conditions are the same as those of Figures 1 and 2.

Mentions: Preliminary, we checked that central treatment with valsartan, an AT1 receptor blocker, or PD123319, an AT2 receptor blocker, only had no obvious effect on plasma levels of Ad (data not shown). Pretreatment with valsartan (100 nmol per animal, i.c.v.) almost abolished AngII- (3 nmol per animal, i.c.v.) induced elevation of plasma Ad (Figure 3a and 3b). On the other hand, pretreatment with PD123319 (100 nmol per animal, i.c.v.) had no significant effect on the AngII-induced response (Figure 3c and 3d). The actual values for Ad at 0 min were 303 ± 22 pg ml−1 in the vehicle-1- [3 μl of 100% N,N-dimethylformamide (DMF) per animal, i.c.v.] pretreated group (n = 5), 118 ± 21 pg ml−1 in the valsartan-pretreated group (n = 5), 184 ± 52 pg ml−1 in the vehicle-2- (5 μl saline per animal, i.c.v.) pretreated group (n = 4) and 148 ± 28 pg ml−1 in the PD123319-pretreated group (n = 6), respectively.


Angiotensin II acting on brain AT 1 receptors induces adrenaline secretion and pressor responses in the rat
Effects of valsartan and PD123319 on the centrally administered AngII-induced elevation of plasma adrenaline levels.Valsartan (Val) (AT1 receptor blocker) (100 nmol per animal), vehicle-1 (3 μl DMF per animal), PD123319 (PD) (AT2 receptor blocker) (100 nmol per animal), or vehicle-2 (5 μl saline per animal) was i.c.v. administered 30 min before the administration of AngII (3 nmol per animal, i.c.v.). (a and c) Increment of plasma adrenaline above the basal level. Arrows indicate the administration of Val (a)/PD (c)/vehicle-1/vehicle-2 and AngII. (b and d) AUC of the elevation of plasma adrenaline above the basal level for each group of (a) and (c), respectively. *P < 0.05, when compared to the vehicle-1- and AngII-treated group with an unpaired Student's t-test. The other conditions are the same as those of Figures 1 and 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5384216&req=5

f3: Effects of valsartan and PD123319 on the centrally administered AngII-induced elevation of plasma adrenaline levels.Valsartan (Val) (AT1 receptor blocker) (100 nmol per animal), vehicle-1 (3 μl DMF per animal), PD123319 (PD) (AT2 receptor blocker) (100 nmol per animal), or vehicle-2 (5 μl saline per animal) was i.c.v. administered 30 min before the administration of AngII (3 nmol per animal, i.c.v.). (a and c) Increment of plasma adrenaline above the basal level. Arrows indicate the administration of Val (a)/PD (c)/vehicle-1/vehicle-2 and AngII. (b and d) AUC of the elevation of plasma adrenaline above the basal level for each group of (a) and (c), respectively. *P < 0.05, when compared to the vehicle-1- and AngII-treated group with an unpaired Student's t-test. The other conditions are the same as those of Figures 1 and 2.
Mentions: Preliminary, we checked that central treatment with valsartan, an AT1 receptor blocker, or PD123319, an AT2 receptor blocker, only had no obvious effect on plasma levels of Ad (data not shown). Pretreatment with valsartan (100 nmol per animal, i.c.v.) almost abolished AngII- (3 nmol per animal, i.c.v.) induced elevation of plasma Ad (Figure 3a and 3b). On the other hand, pretreatment with PD123319 (100 nmol per animal, i.c.v.) had no significant effect on the AngII-induced response (Figure 3c and 3d). The actual values for Ad at 0 min were 303 ± 22 pg ml−1 in the vehicle-1- [3 μl of 100% N,N-dimethylformamide (DMF) per animal, i.c.v.] pretreated group (n = 5), 118 ± 21 pg ml−1 in the valsartan-pretreated group (n = 5), 184 ± 52 pg ml−1 in the vehicle-2- (5 μl saline per animal, i.c.v.) pretreated group (n = 4) and 148 ± 28 pg ml−1 in the PD123319-pretreated group (n = 6), respectively.

View Article: PubMed Central - PubMed

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus