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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.


Effect of AngII on secretion of noradrenaline and adrenaline from cultured bovine adrenal chromaffin cells.Cells were incubated with (3.3 or 10 μM) or without (None) indicated concentrations of AngII for up to 120 min at 37°C. Subsequently, both noradrenaline (a) and adrenaline (b) secreted spontaneously in the incubation medium were measured by HPLC. Data represent the mean ± s.e.m. *P < 0.05, when compared to the “None” group with an unpaired Student's t-test.
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f4: Effect of AngII on secretion of noradrenaline and adrenaline from cultured bovine adrenal chromaffin cells.Cells were incubated with (3.3 or 10 μM) or without (None) indicated concentrations of AngII for up to 120 min at 37°C. Subsequently, both noradrenaline (a) and adrenaline (b) secreted spontaneously in the incubation medium were measured by HPLC. Data represent the mean ± s.e.m. *P < 0.05, when compared to the “None” group with an unpaired Student's t-test.

Mentions: In comparison with the control group, the AngII- (3.3 or 10 μM) treated group showed significant increments of spontaneous secretion of NA and Ad from the cultured bovine adrenal chromaffin cells at 60, 90 and 120 min after administration (Figure 4a and 4b). The degree of increments in Ad was larger than those in NA (Figure 4a and 4b).


Angiotensin II acting on brain AT 1 receptors induces adrenaline secretion and pressor responses in the rat
Effect of AngII on secretion of noradrenaline and adrenaline from cultured bovine adrenal chromaffin cells.Cells were incubated with (3.3 or 10 μM) or without (None) indicated concentrations of AngII for up to 120 min at 37°C. Subsequently, both noradrenaline (a) and adrenaline (b) secreted spontaneously in the incubation medium were measured by HPLC. Data represent the mean ± s.e.m. *P < 0.05, when compared to the “None” group with an unpaired Student's t-test.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4: Effect of AngII on secretion of noradrenaline and adrenaline from cultured bovine adrenal chromaffin cells.Cells were incubated with (3.3 or 10 μM) or without (None) indicated concentrations of AngII for up to 120 min at 37°C. Subsequently, both noradrenaline (a) and adrenaline (b) secreted spontaneously in the incubation medium were measured by HPLC. Data represent the mean ± s.e.m. *P < 0.05, when compared to the “None” group with an unpaired Student's t-test.
Mentions: In comparison with the control group, the AngII- (3.3 or 10 μM) treated group showed significant increments of spontaneous secretion of NA and Ad from the cultured bovine adrenal chromaffin cells at 60, 90 and 120 min after administration (Figure 4a and 4b). The degree of increments in Ad was larger than those in NA (Figure 4a and 4b).

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.