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

^*Korrespondierende/r Autor/-in für diese Arbeit

Inst. Exp. Clin. Pharmacol. Toxicol.

8 Zitate (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.

Originalsprache	Englisch
Zeitschrift	Annals of the New York Academy of Sciences
Jahrgang	1009
Seiten (von - bis)	270-273
Seitenumfang	4
ISSN	0077-8923
DOIs	https://doi.org/10.1196/annals.1304.034
Publikationsstatus	Veröffentlicht - 01.01.2003

Strategische Forschungsbereiche und Zentren

Forschungsschwerpunkt: Gehirn, Hormone, Verhalten - Center for Brain, Behavior and Metabolism (CBBM)

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Dieser Output leistet einen Beitrag zu folgendem(n) Ziel(en) für nachhaltige Entwicklung

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10.1196/annals.1304.034

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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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AU - Häuser, Walter

AU - Dominiak, Peter

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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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