Levonordefrin - CAS 829-74-3
Catalog number: 829-74-3
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Adrenergic Receptor
Levonordefrin is a adrenergic receptor agonist and can be used as a topical nasal decongestant and vasoconstrictor in dentistry in the United States. Levonordefrin is also a metabolite of the antihypertensive drug methyldopa.
White to Pale Beige Solid
4-[(1R,2S)-2-Amino-1-hydroxypropyl]-1,2-benzenediol; BA 2818; Corbadrine; D-(-)-Cobefrin; L-α-Methylnoradrenaline; Levonordefrin; Neo-cobefrin; l-Cobefrin; (-)-Nordefrin;
Acidic Aqueous, DMSO (Sparingly)
-20℃ Freezer
decongestant; vasoconstrictor
Quality Standard:
Shelf Life:
2 month in rt, long time
Boiling Point:
No Data Available
Melting Point:
>200℃ (dec.)
Canonical SMILES:
1.Influence of cocaine and sodium on bretylium uptake by reserpine-treated guinea-pig left atrium.
García AG;Sánchez-García P Br J Pharmacol. 1975 Feb;53(2):247-55.
1 The effects of cocaine and sodium on bretylium uptake into sympathetic nerve terminals were investigated in the reserpine-treated guinea-pig left atrium. The ability of bretylium pretreatment to increase the retention of noradrenaline was used as an index of bretylium uptake. Such increased retention has been assessed both by direct measurement and by the ability of tyramine to produce an inotropic response. 2 The restoration of the response to tyramine after incubation with noradrenaline was abolished when the atrium was pretreated with bretylium in the presence of cocaine. When bretylium was added before cocaine, or when alpha-methyl-noradrenaline (not a substrate for monoamine oxidase) was used for incubation, the responses to tyramine were restored in the normal way. 3 Bretylium greatly enhanced the retention of [3-H]-noradrenaline; when bretylium was added in the presence of cocaine, [3-H]-noradrenaline retention was severely impaired. 4 Pretreatment with bretylium in a low-sodium (25 mM) or sodium-free medium significantly decreased the retention of [3-H]-noradrenaline, as compared with the control. 5 Potassium deprivation did not modify the enhanced retention of [3-H]-noradrenaline induced by bretylium pretreatment.
2.On the mechanism of pancuronium-induced supersensitivity to noradrenaline in rat smooth muscle.
Tomlinson DR Br J Pharmacol. 1979 Mar;65(3):473-8.
1. Pancuronium bromide (5 x 10(-5) M) caused supersensitivity to noradrenaline in the rat isolated vas deferens and hepatic portal vein. This supersensitivity was manifest as a parallel leftward shift of the dose-response curve for noradrenaline with no alteration of the maximum response to the agonist. 2. Pancuronium did not potentiate the response of the vas and portal vein to St 91, an alpha-adrenoceptor agonist which is not a substrate for Uptake1. 3. Pancuronium did not potentiate the response of the vas to CaCl2. 4. In vasa deferentia made supersensitive to noradrenaline by treatment with cocaine (1 x 10(-5) M) pancuronium induced no further potentiation of the response to noradrenaline. However, the supersensitivity to noradrenaline induced by pancuronium alone was augmented by the addition of cocaine. 5. Histofluorescence studies showed that pancuronium inhibited neuronal uptake of alpha-methyl noradrenaline in various noradrenergically-innervated tissues from reserpine-treated rats. 6. This study, with support from the literature, suggests that pancuronium induces noradrenaline supersensitivity by blockade of Uptake1.
3.Centrally acting antihypertensive drugs. Present and future.
van Zwieten PA Clin Exp Hypertens. 1999 Jul-Aug;21(5-6):859-73.
The classic centrally acting antihypertensives such as clonidine, guanfacine and alpha-methyl-DOPA (via its active metabolite alpha-methyl-noradrenaline) induce peripheral sympathoinhibition and a fall in blood pressure as a result of alpha2-adrenoceptor stimulation in the brain stem. These drugs have lost much of their clinical importance because of their unfavourable side-effects (sedation, dry mouth, impotence), which are also mediated by alpha2-adrenoceptors, although in other anatomical regions. Moxonidine and rilmenidine are the examples of a new class of centrally acting antihypertensives, which cause peripheral sympathoinhibition mediated by imidazoline (I1)-receptors in the rostral ventromedulla (RVLM). Their side-effect profile appears to be better than that of clonidine and alpha-methyl-DOPA, probably because of a weaker affinity for alpha2-adrenoceptors. The mode of action, haemodynamic profile, antihypertensive efficacy and adverse reactions of the classic and newer centrally acting antihypertensives are the subject of the present survey. Attention is also paid to other therapeutic applications of centrally acting antihypertensives, such as congestive heart failure and the metabolic syndrome.
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CAS 829-74-3 Levonordefrin

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