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Rilmenidine Sale

(Synonyms: 利美尼啶) 目录号 : GC60325

An antihypertensive agent

Rilmenidine Chemical Structure

Cas No.:54187-04-1

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产品描述

Rilmenidine is an antihypertensive agent.1 It binds to imidazole receptors in bovine rostral ventrolateral medulla homogenates (Ki = 6.1 nM), as well as α2-adrenergic receptors in bovine prefrontal cortex homogenates (Ki = 87 nM). Rilmenidine induces hypotension and bradycardia in anesthetized rats (ED50s = 0.25 and 0.35 mg/kg, respectively). It also reduces mean arterial pressure and renal sympathetic nerve activity in a rabbit model of renal hypertension induced by a renal artery clip when administered at a dose of 2.5 mg/kg.2 Rilmenidine (1 ?M) increases levels of LC3-II, a marker of autophagy, in PC12 cells.3 Formulations containing rilmenidine have been used in the treatment of hypertension.

1.Gomez, R.E., Ernsbarger, P., Feinland, G., et al.Rilmenidine lowers arterial pressure via imidazole receptors in brainstem C1 areaEur. J. Pharmacol.195(2)181-191(1991) 2.Burke, S.L., Evans, R.G., and Head, G.A.Effects of chronic sympatho-inhibition on renal excretory function in renovascular hypertensionJ. Hypertens.29(5)945-952(2011) 3.Williams, A., Sarkar, S., Cuddon, P., et al.Novel targets for Huntington's disease in an mTOR-independent autophagy pathwayNat. Chem. Biol.4(5)295-305(2008)

Chemical Properties

Cas No. 54187-04-1 SDF
别名 利美尼啶
Canonical SMILES C1(NC(C2CC2)C3CC3)=NCCO1
分子式 C10H16N2O 分子量 180.25
溶解度 DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 30 mg/ml,Ethanol:PBS (pH 7.2) (1:6): 0.14 mg/ml 储存条件
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1 mM 5.5479 mL 27.7393 mL 55.4785 mL
5 mM 1.1096 mL 5.5479 mL 11.0957 mL
10 mM 0.5548 mL 2.7739 mL 5.5479 mL
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Research Update

Rilmenidine: a clinical overview

Am J Hypertens 2000 Jun;13(6 Pt 2):106S-111S.PMID:10921529DOI:10.1016/s0895-7061(00)00226-0.

Rilmenidine is an antihypertensive agent with selectivity for I1 imidazoline receptors that acts both centrally by reducing sympathetic overactivity and in the kidney by inhibiting the Na+/H+ antiport. Rilmenidine provides antihypertensive efficacy comparable with that of diuretics, beta-blockers, calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors. Experience from trials and clinical practice highlights Rilmenidine's clinical and metabolic acceptability in hypertensive populations, including those at special risk because of old age, renal impairment, diabetes mellitus, or dyslipidemia. In the at-risk hypertensive, Rilmenidine reduces left ventricular hypertrophy to a similar degree to other reference agents. New studies show a significant improvement in glucose metabolism in metabolic syndrome patients treated with Rilmenidine, and a significant reduction in microalbuminuria during Rilmenidine treatment of hypertensive type 2 diabetics. Thus the efficacy/tolerance ratio of Rilmenidine supports its role as a first-line antihypertensive option for all groups of hypertensive patient, with specific advantages in some at-risk populations.

Rilmenidine: a novel antihypertensive agent

Am J Med 1989 Sep 18;87(3C):24S-29S.PMID:2571292DOI:10.1016/0002-9343(89)90501-9.

Rilmenidine is a novel antihypertensive agent related to alpha 2-agonists. Pharmacologic and clinical data concerning efficacy and acceptability of Rilmenidine, its effects on physiologic functions, and hypothesis of mechanism of action are described in this report. The dominant aspect of Rilmenidine is the observed dissociation at therapeutic doses between antihypertensive and central effects. In this respect, several findings resulting from fundamental pharmacology, clinical pharmacology, and therapeutics differentiate Rilmenidine from clonidine and related drugs. Hypotheses to explain the results observed with Rilmenidine involve unknown properties that could counteract with the alpha 2-adrenoceptor-mediated sedation, respective contribution of central and peripheral components to the activity of Rilmenidine, and possible contribution of imidazoline receptors.

Recent advances in the pharmacology of Rilmenidine

Am J Med 1989 Sep 18;87(3C):14S-17S.PMID:2571291DOI:10.1016/0002-9343(89)90499-3.

The antihypertensive properties of Rilmenidine, an oxazoline derivative, have been demonstrated in several experimental models of hypertension after short- or long-term administration. In pentobarbitone-anesthetized spontaneously hypertensive rats, intravenous Rilmenidine (0.1 to 1 mg/kg) dose-dependently reduced blood pressure and heart rate. Upon long-term subcutaneous infusion (5 to 15 mg/kg per day) in conscious spontaneously hypertensive rats, Rilmenidine induced a dose-dependent decrease in both cardiovascular parameters. In conscious sino-aortic denervated dogs, Rilmenidine (1 mg/kg orally for two weeks) significantly reduced blood pressure and heart rate. The hypotensive action of Rilmenidine is mediated through a reduction in peripheral sympathetic tone, resulting from a central action and possibly a peripheral action. Rilmenidine also decreases catecholamine release from the adrenal medulla which might contribute to the antihypertensive effect. Therefore, Rilmenidine acts similarly to clonidine and related compounds in order to lower blood pressure, i.e., reduction of sympathetic tone. Nevertheless, although it binds to alpha 2-adrenoceptors, Rilmenidine did not cause sedation in animal models: at doses up to 10 mg/kg in mice and rats, it did not prolong the barbiturate-induced sleeping time and did not modify the spontaneous locomotor activity in rats at doses up to 2.5 mg/kg. These results demonstrate a dissociation between sedative and antihypertensive effects of Rilmenidine. Three hypotheses have been proposed to explain why this drug is almost devoid of sedative activity in animal experimental models: (1) unknown properties counteracting the alpha 2-adrenoceptor-mediated sedation; (2) a preferential action at the peripheral level; (3) central receptors involved in sedation and hypotension may be different. The intimate mechanism underlying the hypotensive effects of Rilmenidine is currently under investigation. The evidence for Rilmenidine binding on central sites named "imidazoline sites" involved in blood pressure regulation could possibly provide further insight into its mechanism of action and explain the duality of its effects.

Distinctive features of Rilmenidine possibly related to its selectivity for imidazoline receptors

Am J Hypertens 1992 Apr;5(4 Pt 2):91S-98S.PMID:1350732DOI:10.1093/ajh/5.4.91s.

Rilmenidine is an oxazoline derivative with antihypertensive activity which was developed to enhance the dissociation between the hypotensive and adverse effect profile of centrally acting agents. Experimental studies have indicated that Rilmenidine is selective for both alpha 2-adrenoceptors (v alpha 1) and newly discovered nonadrenergic imidazoline receptors in the brain and in the periphery. In experimental studies, Rilmenidine differs from clonidine in that it is more selective for imidazoline receptors than for alpha 2-adrenoceptors; at equihypotensive doses, Rilmenidine causes less bradycardia and reduction in cardiac output, less sedation, and little or no antinociceptive action compared to clonidine. The hypotensive effects of Rilmenidine are antagonised by idazoxan and yohimbine, but idazoxan (imidazoline structure) is six times more potent than yohimbine (a selective alpha 2-antagonist). In isolated renal proximal tubule cells, where imidazoline binding has also been shown, Rilmenidine inhibits reabsorption of sodium. Clinical studies comparing 1 mg Rilmenidine with placebo demonstrated significant reductions in blood pressure (BP) (61% Rilmenidine v 23% placebo normalized to 160/90 mm Hg). The reduction in BP was not associated with classical alpha 2 side effects such as dry mouth or daytime drowsiness. Compared with clonidine (0.15 to 0.3 mg), equihypotensive doses of Rilmenidine (1 to 2 mg) induced two to three times less dry mouth, daytime drowsiness, and constipation; no orthostatic hypotension was reported. Methyldopa (0.5 to 1 mg) v Rilmenidine (1 to 2 mg) indicated a comparable reduction of BP with significantly less weakness, drowsiness, orthostatic dizziness, and dry mouth on Rilmenidine; there was no evidence of the "clonidine withdrawal syndrome" on drug withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)

Rilmenidine: a novel approach to first-line treatment of hypertension

Am J Hypertens 1992 Apr;5(4 Pt 2):99S-105S.PMID:1350733DOI:10.1093/ajh/5.4.99s.

Rilmenidine (RIL) is a novel antihypertensive drug selectively acting at the sites of imidazoline receptors. Compared with diuretics, beta-blockers, Ca2+ antagonists and angiotensin converting enzyme inhibitors, the four major groups recommended by the US Joint National Committee as first-line antihypertensive drugs, RIL appears to meet the same criteria of efficacy, safety, and acceptability. Rilmenidine dose-dependently decreases blood pressure (BP), acting as a vasodilator by decreasing vascular resistance through inhibition of the adrenergic nervous system, even while the BP changes due to standing and exercise. In comparison with placebo, RIL significantly decreased BP. In double-blind comparative trials versus first-line diuretics and beta-blockers, RIL normalized BP in approximately 60% patients, showing a similar efficacy to other drugs. In contrast with hydrochlorothiazide, RIL decreased total cholesterol and did not change plasma potassium levels. No tachyphylaxis was observed during long-term treatment. Central side effects, which have contributed to the limitation of the use of alpha 2-agonists as second- or third-line therapy for hypertension, were significantly less frequent with RIL than with clonidine or methyldopa. Indeed, the incidence of dry mouth and drowsiness during double-blind comparative trials versus clonidine and methyldopa was significantly lower with RIL. This absence of central side-effects was confirmed in double-blind comparative trials versus hydrochlorothiazide and atenolol. In contrast with clonidine, no sodium retention or weight gain were observed during chronic treatment with RIL.(ABSTRACT TRUNCATED AT 250 WORDS)