ArticleJournal of cardiovascular translational research2021
Involvement of Histamine 2 Receptor in Alpha 1 Adrenoceptor Mediated Cardiac Hypertrophy and Oxidative Stress in H9c2 Cardio Myoblasts.
Article in Journal of cardiovascular translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 6 citations in OpenAlex.
- Inhibitors of gastric acid secretion increase oxidative stress and matrix metalloproteinase-2 activity leading to vascular remodeling.Molecular and cellular biochemistry · 2024Article
- Famotidine promotes inflammation by triggering cell pyroptosis in gastric cancer cells.BMC pharmacology & toxicology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the involvement of ɑ1adrenergic (ɑ1AR) and Histamine 2 receptors (H2R) in cardiac hypertrophy (CH), their relationship is yet to be studied. Our study investigated interrelationship between them using in vitro CH model. H9c2 cardiomyoblasts were exposed to phenylephrine (ɑ1AR agonist-50 μM) in the presence, the absence of famotidine (H2R antagonist-10 μM) and BAY 11-7082 (NF-kB inhibitor-10 μM). The impact of ɑ1AR stimulation on H2R expression and oxidative stress was assessed. Hypertrophic indices were assessed from activities of enzymatic mediators of cardiac hypertrophy, total protein content, BNP levels and cell volume. Additionally, the inverse agonistic property of famotidine and NFkB activity was also studied. ɑ1AR-induced H2R expression, oxidative stress and hypertrophic indices were significantly abolished by famotidine and pharmacological inhibitor of NFkB. Increase in constitutive activity of H2R was noticed correlating with increased receptor population. These results suggest involvement of NFkB-mediated upregulation of H2R in ɑ1AR-mediated CH.
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