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Cited by 117Renin-Angiotensin System StudiesCardiovascular, Neuropeptides, and Oxidative Stress ResearchEicosanoids and Hypertension Pharmacology

The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.

Angiotensin II increases norepinephrine release from atria by acting on angiotensin subtype 1 receptors.

Brasch, H, Sieroslawski, L, Dominiak, P·1993·Hypertension
DOI 10.1161/01.hyp.22.5.699
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Abstract

Norepinephrine stores in electrically driven guinea pig isolated atria were loaded with [3H]norepinephrine, and norepinephrine release was deduced from the radioactivity efflux. Electrical field stimulation of sympathetic nerve endings was applied during the refractory period of atrial contractions. The stimulation-induced release of norepinephrine was increased by angiotensin II (Ang II) (10(-8) to 10(-6) mol/L) in a concentration-dependent manner. The maximum observed effect was a 55% augmentation. The effects of 10(-7) and 10(-6) mol/L Ang II were abolished by 10(-6) and 10(-5) mol/L of the subtype 1 Ang II receptor antagonist losartan, respectively. Losartan by itself (10(-6) mol/L) caused a 14% reduction of norepinephrine release. The subtype 2 Ang II receptor ligand PD 123319 (1-[[4-(dimethylamino)-3-methylphenyl]methyl]-5-(diphenylacetyl)- 4,5,6,7-tetrahydro-1H-imidazo[4,5-c]pyridine-6-carboxylic acid ditrifluoroacetate) in a concentration of 10(-4) mol/L had no detectable influence on transmitter release and did not antagonize the effect of Ang II. Angiotensin I (10(-6) and 10(-5) mol/L) increased norepinephrine release maximally by 23%. This effect was antagonized by 10(-5) mol/L losartan and did not appear in the presence of 10(-6) mol/L of the converting enzyme inhibitor ramiprilat. These results suggest that Ang II increases norepinephrine release by an activation of subtype 1 receptors, whereas angiotensin I is converted to Ang II to become effective.

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Crossref · 10.1161/01.hyp.22.5.699

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Metadata

Authors
Brasch, H., Sieroslawski, L., & Dominiak, P.
Affiliations
University of Lübeck (DE)
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1993-11
Volume
22
Issue
5
Pages
699-704
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
DOI
10.1161/01.hyp.22.5.699
OpenAlex
W2131304527
Cited by
117
References
39
Citations by year
2026: 1 · 2021: 1 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 2 · 2012: 1
FWCI
3.95
Type
journal article
Language
en
Open access
closed
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
angiotensin II, noradrenaline release, atrium, angiotensin II type 1 receptor, angiotensin I, losartan, PD123319, sympathetic activation, electrical field stimulation, ramiprilat, renin-angiotensin system
MeSH terms
Analysis of Variance, Angiotensin I, Angiotensin II, Angiotensin-Converting Enzyme Inhibitors, Animals, Biphenyl Compounds, Dose-Response Relationship, Drug, Guinea Pigs, Heart, Heart Atria, Imidazoles, Kinetics, Male, Myocardium, Norepinephrine, Receptors, Angiotensin, Tetrazoles, Ramipril, Losartan, Angiotensin Receptor Antagonists, In Vitro Techniques

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