Urapidil
(Synonyms: 乌拉地尔) 目录号 : GC37861
An α1-AR antagonist and 5-HT1A receptor partial agonist
Cas No.:34661-75-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Urapidil is an antagonist of α1-adrenergic receptors (α1-ARs) and a partial agonist of the serotonin (5-HT) receptor subtype 5-HT1A.1,2 It selectively binds to α1- over α2-ARs (IC50s = 0.74 and 42 μM, respectively) and to 5-HT1A over 5-HT1B and 5-HT2 receptors (IC50s = 0.4, 20.4, and >10 μM, respectively) in rat cortex.1 Urapidil inhibits cAMP accumulation induced by forskolin in calf hippocampus as a functional model for 5-HT1A receptors (EC50 = 390 nM).3 It is also a β1-AR antagonist that inhibits the positive chronotropic response induced by isoproterenol in isolated rat atria (pA2 = 6.05).4 Urapidil (1 μmol/kg, i.v.) lowers mean arterial pressure (MAP) in anesthetized cats, an effect that is reduced by central administration of the 5-HT1A receptor antagonist spiroxatrine.5
1.Gross, G., Hanft, G., and Kolassa, N.Urapidil and some analogues with hypotensive properties show high affinities for 5-hydroxytryptamine (5-HT) binding sites of the 5-HT1A subtype and for α1-adrenoceptor binding sitesNaunyn Schmiedebergs Arch Pharmacol.336(6)597-601(1987) 2.van Zwieten, P.A.Pharmacologic profile of urapidilAm. J. Cardiol.64(7)1D-6D(1989) 3.Schoeffter, P., and Hoyer, D.Centrally acting hypotensive agents with affinity for 5-HT1A binding sites inhibit forskolin-stimulated adenylate cyclase activity in calf hippocampusBr. J. Pharmacol.95(3)975-985(1988) 4.Verberne, A.J., and Rand, M.J.Effect of urapidil on β-adrenoceptors of rat atriaEur. J. Pharmacol.108(2)193-196(1985) 5.Kolassa, N., Beller, K.D., and Sanders, K.H.Involvement of brain 5-HT1A receptors in the hypotensive response to urapidilAm. J. Cardiol.64(7)7D-10D(1989)
| Cas No. | 34661-75-1 | SDF | |
| 别名 | 乌拉地尔 | ||
| Canonical SMILES | O=C1N(C)C(C=C(NCCCN2CCN(C3=CC=CC=C3OC)CC2)N1C)=O | ||
| 分子式 | C20H29N5O3 | 分子量 | 387.48 |
| 溶解度 | DMSO: 25 mg/mL (64.52 mM); Water: < 0.1 mg/mL (insoluble) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.5808 mL | 12.9039 mL | 25.8078 mL |
| 5 mM | 0.5162 mL | 2.5808 mL | 5.1616 mL |
| 10 mM | 0.2581 mL | 1.2904 mL | 2.5808 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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工作液浓度： mg/ml；
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1. 首先保证母液是澄清的；
2.
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Urapidil. A reappraisal of its use in the management of hypertension
Drugs 1998 Nov;56(5):929-55.PMID:9829161DOI:10.2165/00003495-199856050-00016.
Urapidil is a peripheral postsynaptic alpha 1-adrenoceptor antagonist with central agonistic action at serotonin 5-HT1A receptors. It reduces blood pressure by decreasing peripheral vascular resistance. Oral Urapidil decreases blood pressure in patients with mild to moderate essential hypertension and associated risk factors such as hyperlipidaemia or type 2 (non-insulin-dependent) diabetes mellitus with no effect on heart rate. The antihypertensive efficacy of Urapidil is similar to that of most comparators in patients with mild to moderate essential or secondary hypertension and no concomitant risk factors. However, the antihypertensive efficacy of Urapidil was lower than that of hydrochlorothiazide in a well designed trial. Lipid levels and glucose metabolism are not adversely affected and may improve with Urapidil in patients with lipid or glucose abnormalities. Urapidil can be safely combined with other antihypertensive agents such as hydrochlorothiazide and nifedipine and improves blood pressure control in previous nonresponders to monotherapy. Intravenous Urapidil reduces blood pressure in patients with pre-eclampsia or hypertension in pregnancy and in patients with hypertensive crises or peri- or postoperative hypertension. The decrease in blood pressure is similar to that observed after nifedipine, enalaprilat, sodium nitroprusside and dihydralazine, greater than that of ketanserin according to 1 larger study, and greater than that of sublingual nitroglycerin in 1 trial in patients with nonsurgical hypertensive crises and pulmonary oedema. However, more patients responded to treatment with Urapidil than with enalaprilat or nifedipine. Heart rate is less likely to be altered by Urapidil than with some comparator drugs. Urapidil appears to be well tolerated, with most adverse events being mild and transient. The incidence of adverse events with Urapidil is similar to that with prazosin, metoprolol, atenolol, sodium nitroprusside and hydrochlorothiazide and less than that with nifedipine and clonidine. Urapidil may not be as well tolerated as captopril and, in 1 study, more Urapidil than nitrendipine recipients discontinued treatment because of adverse events. Conclusions: Urapidil reduces blood pressure without altering heart rate. The oral formulation is an effective choice in patients with hypertension and concomitant dyslipidaemia or type 2 diabetes mellitus, in whom the drug does not adversely affect and may improve lipid profiles and glucose metabolism. The intravenous formulation is effective in controlling various hypertensive crises and hypertension associated with pregnancy or surgery and is similar to or better than other first-line agents used in these conditions. Thus, Urapidil may be a useful alternative to currently available antihypertensive agents.
Urapidil: an unknown / known antihypertensive
Vnitr Lek 2022 Fall;68(4):253-256.PMID:36220424doi
Essential arterial hypertension is not a disease that would significantly adversely affect patients in their daily activities. At least mostly. Nonetheless, it has a significant negative impact on cardiovascular morbidity and mortality. The tight correlation with the degree of hypertension, the patients age and, of course, commorbidities and cardiovascular risk factors is obvious. Therefore, the goal of hypertensive therapy is not only to try to achieve optimal reduction of blood pressure, but in a broader sense to reduce the risk of the just mentioned consequences, i.e. to reduce morbidity and reduce mortality. The antihypertensive drug Urapidil can also be used in pharmacotherapy, the brief description of which is the subject of this article.
Urapidil in the treatment of hypertension
Drugs 1988;35 Suppl 6:188-92.PMID:3042358DOI:10.2165/00003495-198800356-00025.
Urapidil is an alpha 1-adrenoceptor antagonist which also has a central antihypertensive effect, the mechanism of which has yet to be conclusively defined. A number of open and comparative studies have produced evidence for the efficacy and safety of Urapidil. A study recently completed by the author produced a dose-dependent antihypertensive effect of Urapidil which, however, failed to achieve statistical significance, probably due to a large variance of the data and an unexpectedly large placebo effect. Adverse reactions are those expected from an alpha 1-blocker, particularly dizziness, as well as nausea and fatigue. Urapidil is potentially an important new antihypertensive agent; further variable dose and combination (with other antihypertensive agents) studies would help further define its therapeutic niche.
Urapidil, a multiple-action alpha-blocking drug
Am J Cardiol 1989 Aug 15;64(7):11D-15D.PMID:2569263DOI:10.1016/0002-9149(89)90689-9.
Investigations in animals indicate that Urapidil has a number of actions that may be relevant to its antihypertensive effect. It has an alpha 1-blocking action, a weak beta 1-blocking effect, an interaction with a serotonin receptor and a central depression of sympathetic tone. Urapidil is well absorbed orally with a bioavailability of about 70% and a time to peak concentration of about 4 hours after a sustained release capsule. It is metabolized in the liver at a half-life of 4.7 hours. Peripheral alpha 1-blocking activity has been demonstrated in humans. A shift to the right in the dose-response curve to phenylephrine has been found after Urapidil, whereas responses to angiotensin are not affected. Evidence for beta 1-blocking activity is marginal. Urapidil does not inhibit the exercise increase in heart rate. Some investigators have suggested a possible inhibition of isoprenaline tachycardia; others have found no evidence. There is some evidence suggestive of a central action of Urapidil in humans as lower single doses result in a decrease in blood pressure and an increase in heart rate. With higher doses the hypotensive effect continues but the tachycardia no longer occurs. However, Urapidil has been reported to increase noradrenaline levels, although there has been a report with a high dose reducing vanillylmandelic acid excretion. Evidence for changes in renin is inconsistent. Hemodynamic studies have revealed findings that are compatible with peripheral alpha 1 blockade. After intravenous administration, peripheral resistance is reduced along with arterial pressure, and cardiac output is increased.(ABSTRACT TRUNCATED AT 250 WORDS)
Urapidil, a dual-acting antihypertensive agent: Current usage considerations
Adv Ther 2010 Jul;27(7):426-43.PMID:20652659DOI:10.1007/s12325-010-0039-0.
Despite the availability of a wide range of effective blood pressure (BP)-lowering agents, a substantial proportion of patients with hypertension fail to achieve target BP levels. The majority of patients with hypertension need a combination of two or more drugs to achieve BP targets and choice of second-line or subsequent-line therapy is an important consideration in hypertension management. Alpha-1-adrenoreceptor antagonists (alpha-blockers) have a BP-lowering effect broadly similar to the other antihypertensive drug classes and are effective as add-on therapy in patients with inadequately controlled hypertension. Alpha-blockers may also have therapeutic benefits that go beyond BP control, including improvements in lipid profile and glucose metabolism, as well as reducing the symptoms of benign prostatic hyperplasia. Urapidil has an alpha-blocking effect but, unlike other alpha-blockers, also has a central sympatholytic effect mediated via stimulation of serotonin 5HT(1A) receptors in the central nervous system. Several studies have suggested that oral Urapidil is effective and well tolerated when used as second-line therapy in patients with BP inadequately controlled with other agents. Urapidil has also been shown to improve glucose and lipid metabolism in hypertensive patients with concomitant diabetes and/or hyperlipidemia. Intravenous Urapidil is effective in the treatment of hypertensive crises, perioperative hypertension, and pre-eclampsia and may have a potential role in the management of acute stroke. In this review, the use of alpha-blockers in hypertension is discussed, with particular focus on Urapidil for the lowering of BP in a variety of clinical settings.