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

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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.


Effects of centrally administered angiotensin II (AngII) on plasma noradrenaline and adrenaline levels.Vehicle (10 μl saline per animal) or AngII (1, 3 or 10 nmol per animal) was i.c.v. administered. (a) Increments of plasma noradrenaline and adrenaline above the basal level. ΔNoradrenaline and ΔAdrenaline: increments of noradrenaline and adrenaline above the basal level are expressed as pg ml−1. Arrow indicates the administration of vehicle or AngII. (b) The area under the curve (AUC) of the elevation of plasma noradrenaline and adrenaline above the basal level for each group is expressed as pg 2 h−1. Each point represents the mean ± s.e.m. *P < 0.05, when compared to the vehicle-treated group with the Bonferroni method.
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f1: Effects of centrally administered angiotensin II (AngII) on plasma noradrenaline and adrenaline levels.Vehicle (10 μl saline per animal) or AngII (1, 3 or 10 nmol per animal) was i.c.v. administered. (a) Increments of plasma noradrenaline and adrenaline above the basal level. ΔNoradrenaline and ΔAdrenaline: increments of noradrenaline and adrenaline above the basal level are expressed as pg ml−1. Arrow indicates the administration of vehicle or AngII. (b) The area under the curve (AUC) of the elevation of plasma noradrenaline and adrenaline above the basal level for each group is expressed as pg 2 h−1. Each point represents the mean ± s.e.m. *P < 0.05, when compared to the vehicle-treated group with the Bonferroni method.

Mentions: Treatment with vehicle [10 μl saline per animal, intracerebroventricularly (i.c.v.)] had no effect on the plasma levels of NA and Ad (Figure 1a and 1b). AngII (1 and 3 nmol per animal, i.c.v.) dose-dependently elevated plasma Ad, but AngII at a dose of 10 nmol per animal (i.c.v.) showed similar effects on plasma Ad compared with the effects of AngII at 3 nmol (Figure 1a and 1b). The Ad responses peaked at 10 min after the administration of AngII and then declined towards their basal levels (Figure 1a). On the other hand, AngII (1, 3 and 10 nmol per animal, i.c.v.) had no significant effects on plasma NA (Figure 1a and 1b). The actual values for NA and Ad at 0 min were 413 ± 21 and 253 ± 14 pg ml−1 (n = 23).


Angiotensin II acting on brain AT 1 receptors induces adrenaline secretion and pressor responses in the rat
Effects of centrally administered angiotensin II (AngII) on plasma noradrenaline and adrenaline levels.Vehicle (10 μl saline per animal) or AngII (1, 3 or 10 nmol per animal) was i.c.v. administered. (a) Increments of plasma noradrenaline and adrenaline above the basal level. ΔNoradrenaline and ΔAdrenaline: increments of noradrenaline and adrenaline above the basal level are expressed as pg ml−1. Arrow indicates the administration of vehicle or AngII. (b) The area under the curve (AUC) of the elevation of plasma noradrenaline and adrenaline above the basal level for each group is expressed as pg 2 h−1. Each point represents the mean ± s.e.m. *P < 0.05, when compared to the vehicle-treated group with the Bonferroni method.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1: Effects of centrally administered angiotensin II (AngII) on plasma noradrenaline and adrenaline levels.Vehicle (10 μl saline per animal) or AngII (1, 3 or 10 nmol per animal) was i.c.v. administered. (a) Increments of plasma noradrenaline and adrenaline above the basal level. ΔNoradrenaline and ΔAdrenaline: increments of noradrenaline and adrenaline above the basal level are expressed as pg ml−1. Arrow indicates the administration of vehicle or AngII. (b) The area under the curve (AUC) of the elevation of plasma noradrenaline and adrenaline above the basal level for each group is expressed as pg 2 h−1. Each point represents the mean ± s.e.m. *P < 0.05, when compared to the vehicle-treated group with the Bonferroni method.
Mentions: Treatment with vehicle [10 μl saline per animal, intracerebroventricularly (i.c.v.)] had no effect on the plasma levels of NA and Ad (Figure 1a and 1b). AngII (1 and 3 nmol per animal, i.c.v.) dose-dependently elevated plasma Ad, but AngII at a dose of 10 nmol per animal (i.c.v.) showed similar effects on plasma Ad compared with the effects of AngII at 3 nmol (Figure 1a and 1b). The Ad responses peaked at 10 min after the administration of AngII and then declined towards their basal levels (Figure 1a). On the other hand, AngII (1, 3 and 10 nmol per animal, i.c.v.) had no significant effects on plasma NA (Figure 1a and 1b). The actual values for NA and Ad at 0 min were 413 ± 21 and 253 ± 14 pg ml−1 (n = 23).

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.