Norepinephrine Release Is Reduced by I1-Receptors in Addition to α2-Adrenoceptors

Walter Raasch; Britta Jungbluth; Ulrich Schäfer; Walter Häuser; Peter Dominiak

doi:10.1196/annals.1304.034

Norepinephrine Release Is Reduced by I₁-Receptors in Addition to α₂-Adrenoceptors

Walter Raasch^*, Britta Jungbluth, Ulrich Schäfer, Walter Häuser, Peter Dominiak

^*Corresponding author for this work

Inst. Exp. Clin. Pharmacol. Toxicol.

10 Citations (Scopus)

Abstract

In pithed spontaneous hypertensive rats, noradrenaline overflow was diminished by moxonidine even when α2-adrenoceptors were blocked quantitatively using phenoxybenzamine, suggesting an I₁-receptor- mediated mechanism of noradrenaline release. This hypothesis was confirmed, since the noradrenaline overflow was (1) increased under α2-adrenoceptors blockade by the mixed I₁/α₂-antagonists efaroxan or idazoxan, (2) still reduced by moxonidine when both α₂- and I₁-receptors were blocked, and (3) diminished by agmatine after pretreatment with phenoxybenzamine, but not with AGN192403. An indirect ganglionic I₁-receptor-mediated mechanism of noradrenaline release is supposed.

Original language	English
Journal	Annals of the New York Academy of Sciences
Volume	1009
Pages (from-to)	270-273
Number of pages	4
ISSN	0077-8923
DOIs	https://doi.org/10.1196/annals.1304.034
Publication status	Published - 01.01.2003

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Research Areas and Centers

Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

Access to Document

10.1196/annals.1304.034

Cite this

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title = "Norepinephrine Release Is Reduced by I1-Receptors in Addition to α2-Adrenoceptors",

abstract = "In pithed spontaneous hypertensive rats, noradrenaline overflow was diminished by moxonidine even when α2-adrenoceptors were blocked quantitatively using phenoxybenzamine, suggesting an I1-receptor- mediated mechanism of noradrenaline release. This hypothesis was confirmed, since the noradrenaline overflow was (1) increased under α2-adrenoceptors blockade by the mixed I1/α2-antagonists efaroxan or idazoxan, (2) still reduced by moxonidine when both α2- and I1-receptors were blocked, and (3) diminished by agmatine after pretreatment with phenoxybenzamine, but not with AGN192403. An indirect ganglionic I1-receptor-mediated mechanism of noradrenaline release is supposed.",

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T1 - Norepinephrine Release Is Reduced by I1-Receptors in Addition to α2-Adrenoceptors

AU - Raasch, Walter

AU - Jungbluth, Britta

AU - Schäfer, Ulrich

AU - Häuser, Walter

AU - Dominiak, Peter

PY - 2003/1/1

Y1 - 2003/1/1

N2 - In pithed spontaneous hypertensive rats, noradrenaline overflow was diminished by moxonidine even when α2-adrenoceptors were blocked quantitatively using phenoxybenzamine, suggesting an I1-receptor- mediated mechanism of noradrenaline release. This hypothesis was confirmed, since the noradrenaline overflow was (1) increased under α2-adrenoceptors blockade by the mixed I1/α2-antagonists efaroxan or idazoxan, (2) still reduced by moxonidine when both α2- and I1-receptors were blocked, and (3) diminished by agmatine after pretreatment with phenoxybenzamine, but not with AGN192403. An indirect ganglionic I1-receptor-mediated mechanism of noradrenaline release is supposed.

AB - In pithed spontaneous hypertensive rats, noradrenaline overflow was diminished by moxonidine even when α2-adrenoceptors were blocked quantitatively using phenoxybenzamine, suggesting an I1-receptor- mediated mechanism of noradrenaline release. This hypothesis was confirmed, since the noradrenaline overflow was (1) increased under α2-adrenoceptors blockade by the mixed I1/α2-antagonists efaroxan or idazoxan, (2) still reduced by moxonidine when both α2- and I1-receptors were blocked, and (3) diminished by agmatine after pretreatment with phenoxybenzamine, but not with AGN192403. An indirect ganglionic I1-receptor-mediated mechanism of noradrenaline release is supposed.

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