Isoprenaline HCl - CAS 51-30-9
Catalog number: B0084-350898
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Adrenergic Receptor
Isoprenaline is a non-selective beta-adrenergic receptor agonist, used for the treatment of bradycardia and heart block. It would increase cAMP levels and activate protein kinase A and ERK1/2 through its effect on β-adrenoceptor.
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B0084-350898 50 g $279 In stock
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Brife Description:
beta-adrenergic receptor agonist, bradycardia and heart block
NCI-c55630; Aerolone; Aerotrol; 4-[1-hydroxy-2-(propan-2-ylamino)ethyl]benzene-1,2-diol, hydrochloride
the treatment of bradycardia and heart block
Canonical SMILES:
1.Isoproterenol directs hair follicle-associated pluripotent (HAP) stem cells to differentiate in vitro to cardiac muscle cells which can be induced to form beating heart-muscle tissue sheets.
Yamazaki A1, Yashiro M1, Mii S1, Aki R1, Hamada Y1, Arakawa N1, Kawahara K2,3, Hoffman RM4,5, Amoh Y1. Cell Cycle. 2016 Mar 3;15(5):760-5. doi: 10.1080/15384101.2016.1146837.
Nestin-expressing hair-follicle-associated pluripotent (HAP) stem cells are located in the bulge area of the follicle. Previous studies have shown that HAP stem cells can differentiate to neurons, glia, keratinocytes, smooth muscle cells, and melanocytes in vitro. HAP stem cells effected nerve and spinal cord regeneration in mouse models. Recently, we demonstrated that HAP stem cells differentiated to beating cardiac muscle cells. The differentiation potential to cardiac muscle cells was greatest in the upper part of the follicle. The beat rate of the cardiac muscle cells was stimulated by isoproterenol. In the present study, we observed that isoproterenol directs HAP stem cells to differentiate to cardiac muscle cells in large numbers in culture compared to HAP stem cells not supplemented with isoproterenol. The addition of activin A, bone morphogenetic protein 4, and basic fibroblast growth factor, along with isoproternal, induced the cardiac muscle cells to form tissue sheets of beating heart muscle cells.
2.ECL cells involvement in the isoproterenol-induced gastroprotection. An ultrastructural study.
Dabroś W1, Brzozowski T, Konturek SJ, Stachura J. Pol J Pathol. 1998;49(1):3-13.
The central and peripheral adrenergic systems are involved in the regulation of several functions in the gut including the maintenance of gastric microcirculation and gastric secretion but little is known about the role of the adrenergic system, in particular, beta-adrenoceptors in the phenomenon of gastroprotection. In this study acute gastric lesions were provoked by an intragastric (i.g.) application of 100% ethanol in rats with topical application of isoproterenol (ISO) (1 mg/kg) or subcutaneous (s.c.) administration of ranitidine (RAN) (40 mg/kg) or both. An area of gastric lesions was determined by planimetry, gastric blood flow (GBF) was determined by H2-gas clearance technique and gastric specimens were taken for histology and electron microscopy. It was found that ISO reduced ethanol-induced gastric mucosal lesions and this effect was accompanied by a rise in GBF. In contrast, RAN applied s.c. in a dose that produced almost complete achlorhydria, failed to affect ethanol-lesions but attenuated significantly ISO induced gastroprotection and abolished the increase in the GBF induced by this beta-adrenoceptor agonist.
3.Prolonged isoproterenol infusion impairs the ability of beta(2)-agonists to increase alveolar liquid clearance.
Morgan EE1, Hodnichak CM, Stader SM, Maender KC, Boja JW, Folkesson HG, Maron MB. Am J Physiol Lung Cell Mol Physiol. 2002 Apr;282(4):L666-74.
We determined if prolonged isoproterenol (Iso) infusion in rats impaired the ability of the beta(2)-adrenergic agonist terbutaline to increase alveolar liquid clearance (ALC). We infused rats with Iso (at rates of 4, 40, or 400 or vehicle (0.001 N HCl) for 48 h using subcutaneously implanted miniosmotic pumps. After this time, the rats were anesthetized, and ALC was determined (by mass-balance after instillation of Ringer lactate containing albumin into the lungs) under baseline conditions and after terbutaline administration. Baseline and terbutaline-stimulated ALC in vehicle-infused rats averaged, respectively, 19.6 +/- 1.2% (SE) and 44.7 +/- 1.5%/h. The ability of terbutaline to increase ALC was eliminated at 400, inhibited by 26% at 40 Iso, and was not affected by 4 Iso. beta-adrenergic receptor (betaAR) density of freshly isolated alveolar epithelial type II (ATII) cells from Iso-infused rats was reduced by the 40 and 400 microg.
4.Antioxidant effects of hydroxysafflor yellow A and acetyl-11-keto-β-boswellic acid in combination on isoproterenol-induced myocardial injury in rats.
Chen M1, Wang M1, Yang Q1, Wang M2, Wang Z2, Zhu Y1, Zhang Y1, Wang C1, Jia Y1, Li Y1, Wen A1. Int J Mol Med. 2016 Apr 20. doi: 10.3892/ijmm.2016.2571. [Epub ahead of print]
Oxidative stress plays an important role in the initiation and development of myocardial injury (MI). The peroxisome proliferator-activated receptor gamma coactivator-1α (PGC‑1α)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is considered to be a potential target for cardioprotection in MI. Acetyl-11-keto-β-boswellic acid (AKBA) is the major organic acid component extracted from Boswellia serrata Roxb. ex Colebr. Hydroxysafflor yellow A (HSYA) is the principal active constituent of Carthamus tinctorius L. In the present study, we aimed to investigate the cardioprotective effects of HSYA and AKBA in combination in vivo and in vitro, as well as the underlying mechanisms responsible for these effects. For this purpose, MI was produced in Sprague-Dawley rats by subcutaneous injection with isoproterenol. To model ischemic-like conditions in vitro, H9C2 cells were subjected to oxygen-glucose deprivation (OGD). The levels of creatine kinase-MB (CK‑MB), lactate dehydrogenase (LDH), malondialdehyde (MDA) as well as superoxide dismutase (SOD) activity were examined as well as apoptotic cell death.
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CAS 51-30-9 Isoprenaline HCl

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