Cardiac noradrenaline content is increased by ACE inhibitors due to an AT1-dependent down-regulation of MAO activity

W. Raasch; A. Gieselberg; T. Bartels; A. Dendorfer; P. Dominiak

Cardiac noradrenaline content is increased by ACE inhibitors due to an AT₁-dependent down-regulation of MAO activity

W. Raasch^*, A. Gieselberg, T. Bartels, A. Dendorfer, P. Dominiak

^*Corresponding author for this work

Institute of Experimental and Clinical Pharmacology and Toxicology

Original language	English
Journal	Nieren- und Hochdruckkrankheiten
Volume	31
Issue number	7
Pages (from-to)	281-283
Number of pages	3
ISSN	0300-5224
Publication status	Published - 2002

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 Infection and Inflammation Research (ZIEL)

Cite this

@article{d39c9ce19ad54b45a6c30bc683272991,

title = "Cardiac noradrenaline content is increased by ACE inhibitors due to an AT1-dependent down-regulation of MAO activity",

author = "W. Raasch and A. Gieselberg and T. Bartels and A. Dendorfer and P. Dominiak",

year = "2002",

language = "English",

volume = "31",

pages = "281--283",

journal = "Nieren- und Hochdruckkrankheiten",

issn = "0300-5224",

publisher = "Dustri-Verlag Dr. Karl Feistle",

number = "7",

}

TY - JOUR

T1 - Cardiac noradrenaline content is increased by ACE inhibitors due to an AT1-dependent down-regulation of MAO activity

AU - Raasch, W.

AU - Gieselberg, A.

AU - Bartels, T.

AU - Dendorfer, A.

AU - Dominiak, P.

PY - 2002

Y1 - 2002

UR - https://www.scopus.com/pages/publications/0036311652

M3 - Journal articles

AN - SCOPUS:0036311652

SN - 0300-5224

VL - 31

SP - 281

EP - 283

JO - Nieren- und Hochdruckkrankheiten

JF - Nieren- und Hochdruckkrankheiten

IS - 7

ER -

Cardiac noradrenaline content is increased by ACE inhibitors due to an AT1-dependent down-regulation of MAO activity

UN SDGs

Research Areas and Centers

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Cardiac noradrenaline content is increased by ACE inhibitors due to an AT₁-dependent down-regulation of MAO activity