ArticleInternational journal of cardiology2020
Reversal of angiotensin-(1-12)-caused positive modulation on left ventricular contractile performance in heart failure: Assessment by pressure-volume analysis.
Article in International journal of cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Immunoneutralization of human angiotensin-(1-12) with a monoclonal antibody in a humanized model of hypertension.Peptides · 2022Article
- Chronic GPR30 agonist therapy causes restoration of normal cardiac functional performance in a male mouse model of progressive heart failure: Insights into cellular mechanisms.Life sciences · 2021Article
- The Angiotensin-(1-12)/Chymase axis as an alternate component of the tissue renin angiotensin system.Molecular and cellular endocrinology · 2021Review
- Chronic CaThe Journal of pharmacology and experimental therapeutics · 2021Article
- Angiotensin (1-12) in Humans With Normal Blood Pressure and Primary Hypertension.Hypertension (Dallas, Tex. : 1979) · 2021Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundAngiotensin-(1-12) [Ang-(1-12)] is a renin-independent precursor for direct angiotensin-II production by chymase. Substantial evidence suggests that heart failure (HF) may alter cardiac Ang-(1-12) expression and activity; this novel Ang-(1-12)/chymase axis may be the main source for angiotensin-II deleterious actions in HF. We hypothesized that HF alters cardiac response to Ang-(1-12). Its stimulation may produce cardiac negative modulation and exacerbate left ventricle (LV) systolic and diastolic dysfunction. METHODS AND
resultsWe assessed the effects of Ang-(1-12) (2 nmol/kg/min, iv, 10 min) on LV contractility, LV diastolic filling, and LV-arterial coupling (AVC) in 16 SD male rats with HF-induced by isoproterenol (3 mo after 170 mg/kg sq. for 2 consecutive days) and 10 age-matched male controls. In normal controls, versus baseline, Ang-(1-12) increased LV end-systolic pressure, without altering heart rate, arterial elastance (E
conclusionsIn both normal and HF rats, Ang-(1-12) causes similar vasoconstriction. In normal, Ang-(1-12) increases LV contractile function. In HF, Ang-(1-12) has adverse effects and depresses LV systolic and diastolic functional performance.
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