Propranolol hydrochloride is a nonselective β-adrenergic receptor (βAR) antagonist, has high affinity for the β1AR and β2AR with Ki values of 1.8 nM and 0.8 nM, respectively[1]. Propranolol hydrochloride inhibits [3H]-DHA binding to rat brain membrane preparation with an IC50 of 12 nM[2]. Propranolol hydrochloride is used to control hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy[3].
Propranolol hydrochloride (10-7 M-10-3 M; 24 and 48 hours) increases the total ERK1/2 levels in a dose-dependent manner, and ERK1/2 activation is observed specifically at 10-5 M in HemSCs[4].Propranolol hydrochloride (10-9 M-10-3 M; 24 and 48 hours) significant decreases cell proliferation at 10-4 M propranolol after 24 hours and 10-9 M propranolol after 48 hours in HemSCs[4].Propranolol hydrochloride (50 μM-200 μM; 24 hours) increases Annexin V positivity and caspase-3 activation, rapidly induces HemSC apoptosis[4].
Propranolol hydrochloride (orally administration; 40 mg/kg; daily) significantly reduces the vessel diameter relative to the vehicle-treated implants, and increases the number of cells that expressed phosphorylated ERK1/2 within the IH Matrigel implant[4].
References:
[1]. Galandrin S, et al. Distinct signaling profiles of beta1 and beta2 adrenergic receptor ligands toward adenylyl cyclase and mitogen-activated protein kinase reveals the pluridimensionality of efficacy. Mol Pharmacol. 2006 Nov;70(5):1575-84. Epub 2006 Aug 1
[2]. Briley M, et al. Evidence against beta-adrenoceptor blocking activity of diltiazem, a drug with calcium antagonist properties. Br J Pharmacol. 1980 Aug;69(4):669-73.
[3]. Al-Majed AA, et al. Propranolol. Profiles Drug Subst Excip Relat Methodol. 2017;42:287-338.
[4]. Munabi NC, et al. Propranolol Targets Hemangioma Stem Cells via cAMP and Mitogen-Activated Protein Kinase Regulation. Stem Cells Transl Med. 2016 Jan;5(1):45-55.