Methoxamine Hydrochloride - CAS 61-16-5
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Adrenergic Receptor
Methoxamine Hydrochloride is an alpha-1 adrenergic agonist, similar in structure to butaxamine and 2,5-DMA. It causes prolonged peripheral vasoconstriction. It induces vasoconstriction of skin and splanchnic blood vessels, thus increasing peripheral vascular resistance and raising mean arterial blood pressure. lt is used for the treatment of paroxysmal supraventricular tachycardia and is used as a booster in the state of low blood pressure. It has been listed.
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Solid powder
1-(2,5-Dimethoxyphenyl)-2-aminopropanol;2-Amino-1-(2,5-dimethoxyphenyl)-1-propanolhydrochloride;Alpha-(1-aminoethyl)-2,5-dimethoxy-benzenemethano hydrochloride;Methoxamine HCl;Vasoxyl hydrochloride;2-Amino-1-(2,5-dimethoxyphenyl)propan-1-ol hydrochloride
Soluble in DMSO, not in water
Methoxamine Hydrochloride is used for the treatment of paroxysmal supraventricular tachycardia and is used as a booster in the state of low blood pressure.
Quality Standard:
In-house standard
Kilograms to Tons
Boiling Point:
368.4 °C at 760 mmHg
Melting Point:
212-216 °C
Canonical SMILES:
Current Developer:
Methoxamine Hydrochloride has been listed.
1.Stimulation of calcium-sensing receptors induces endothelium-dependent vasorelaxations via nitric oxide production and activation of IKCa channels.
Greenberg HZ1, Shi J2, Jahan KS2, Martinucci MC2, Gilbert SJ2, Vanessa Ho WS2, Albert AP2. Vascul Pharmacol. 2016 May;80:75-84. doi: 10.1016/j.vph.2016.01.001. Epub 2016 Jan 6.
Stimulation of vascular calcium-sensing receptors (CaSRs) is reported to induce both constrictions and relaxations. However, cellular mechanisms involved in these responses remain unclear. The present study investigates the effect of stimulating CaSRs on vascular contractility and focuses on the role of the endothelium, nitric oxide (NO) and K(+) channels in these responses. In wire myography studies, increasing [Ca(2+)]o from 1mM to 6mM induced concentration-dependent relaxations of methoxamine pre-contracted rabbit mesenteric arteries. [Ca(2+)]o-induced relaxations were dependent on a functional endothelium, and were inhibited by the negative allosteric CaSR modulator Calhex-231. [Ca(2+)]o-induced relaxations were reduced by inhibitors of endothelial NO synthase, guanylate cyclase, and protein kinase G. CaSR activation also induced NO production in freshly isolated endothelial cells (ECs) in experiments using the fluorescent NO indicator DAF-FM.
2.Effects of tempol on altered metabolism and renal vascular responsiveness in fructose-fed rats.
Abdulla MH1, Sattar MA2, Johns EJ1. Appl Physiol Nutr Metab. 2016 Feb;41(2):210-8. doi: 10.1139/apnm-2015-0411. Epub 2015 Nov 5.
This study investigated the effect of tempol (a superoxide dismutase mimetic) on renal vasoconstrictor responses to angiotensin II (Ang II) and adrenergic agonists in fructose-fed Sprague-Dawley rats (a model of metabolic syndrome). Rats were fed 20% fructose in drinking water (F) for 8 weeks. One fructose-fed group received tempol (FT) at 1 mmol·L(-1) in drinking water for 8 weeks or as an infusion (1.5 mg·kg(-1)·min(-1)) intrarenally. At the end of the treatment regimen, the renal responses to noradrenaline, phenylephrine, methoxamine, and Ang II were determined. F rats exhibited hyperinsulinemia, hyperuricemia, hypertriglyceridemia, and hypertension. Tempol reduced blood glucose and insulin levels (all p < 0.05) in FT rats compared with their untreated counterparts. The vasoconstriction response to all agonists was lower in F rats than in control rats by about 35%-65% (all p < 0.05). Vasoconstrictor responses to noradrenaline, phenylephrine, and methoxamine but not Ang II were about 41%-75% higher in FT rats compared with F rats (all p < 0.
3.Pharmacological evidence that NaHS inhibits the vasopressor responses induced by stimulation of the preganglionic sympathetic outflow in pithed rats.
Centurión D1, De la Cruz SH2, Gutiérrez-Lara EJ2, Beltrán-Ornelas JH2, Sánchez-López A2. Eur J Pharmacol. 2016 Jan 5;770:40-5. doi: 10.1016/j.ejphar.2015.11.057. Epub 2015 Nov 28.
It has been reported that i.v. administration of NaHS, a donor of H2S, elicited dose-dependent hypotension although the mechanisms are not completely understood. In this regard, several mechanisms could be involved including the inhibition of the vasopressor sympathetic outflow. Thus, this study was designed to determine the potential capability of NaHS to mediate inhibition of the vasopressor responses induced by preganglionic sympathetic stimulation. For this purpose, Wistar rats were anaesthetised, pithed and cannulated for drug administration. In animals pre-treated with gallamine, the effect of i.v. infusion of NaHS (310 and 560μg/kgmin) or its vehicle (phosphate buffer) was determined on the vasopressor responses induced by: (1) sympathetic stimulation (0.03-10Hz); (2) i.v. bolus injections of exogenous noradrenaline (0.03-3μg/kg); or (3) methoxamine (1-100μg/kg). The vasopressor responses induced by preganglionic sympathetic stimulation were dose-dependently inhibited by i.
4.Endothelial nitric oxide weakens arterial contractile responses and reduces blood pressure during early postnatal development in rats.
Sofronova SI1, Borzykh AA2, Gaynullina DK3, Kuzmin IV4, Shvetsova AA4, Lukoshkova EV5, Tarasova OS4. Nitric Oxide. 2016 Feb 23;55-56:1-9. doi: 10.1016/j.niox.2016.02.005. [Epub ahead of print]
OBJECTIVE: During maturation the vascular system undergoes structural and functional remodeling. At the systemic level it results in a gradual increase of arterial blood pressure during postnatal ontogenesis. The mechanisms of maintaining the blood pressure at a comparatively low level during the early postnatal development are not completely understood. Recently we showed that the hindlimb arteries of young (1-2 wk-old) rats exhibited an enhanced endothelial NO-pathway activity, which weakened their contractile responsiveness compared to the arteries of adult rats. Here we tested the hypothesis that an increased tonic endothelial NO production can take place in the whole vascular system leading to a decreased level of systemic blood pressure in young rats.
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CAS 61-16-5 Methoxamine Hydrochloride

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