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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Abbreviations
- AR:
-
Adrenergic receptors
- BST:
-
Bryostatin 1
- BUR:
-
Burimamide
- Fam:
-
Famotidine
- H2R:
-
Histamine 2 receptor
- PE:
-
Phenylephrine
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The authors would like to acknowledge and show gratitude for the support extended by the National Institute of Pharmaceutical Education and Research, Hyderabad for permitting us to utilize their research facilities.
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Raw Western Blot images. (a-b) the pictorial representation of PRX3 and corresponding Beta actin (c-d)) the pictorial representation of H2R and corresponding Beta actin (PNG 1790 kb)
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Potnuri, A.G., Allakonda, L. & Saheera, S. Involvement of Histamine 2 Receptor in Alpha 1 Adrenoceptor Mediated Cardiac Hypertrophy and Oxidative Stress in H9c2 Cardio Myoblasts. J. of Cardiovasc. Trans. Res. 14, 184–194 (2021). https://doi.org/10.1007/s12265-020-09967-6
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DOI: https://doi.org/10.1007/s12265-020-09967-6