Cardiovascular and central nervous system effects of rilmenidine (S 3341) in rats

Koenig-Berard, Elisabeth; Tierney, Caroline; Beau, Bertrand; Delbarre, Gisèle; Lhoste, F; Labrid, C

doi:10.1016/0002-9149(88)90460-2

Cited by 43 publications

(14 citation statements)

References 28 publications

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“…In comparative studies with clonidine both moxonidine and rilmenidine in antihypertensive doses caused significantly less sedation in various animal models [84,85], thus confirming the concept that clonidine-induced sedation is mediated preferably by central ␣ 2 -adrenoceptors rather than by I 1 -receptors.…”

Section: Pharmacological Characteristics Of Moxonidine and Rilmenidinementioning

confidence: 67%

Central imidazoline (I1) receptors as targets of centrally acting antihypertensives

Zwieten

1997

Journal of Hypertension

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Section: Pharmacological Characteristics Of Moxonidine and Rilmenidinementioning

confidence: 67%

Central imidazoline (I1) receptors as targets of centrally acting antihypertensives

Zwieten

1997

Journal of Hypertension

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“…Rilmenidine does bind, albeit with a lower affinity than clonidine, to alpha2-adrenoceptors and therefore side effects via this receptor cannot be excluded at higher concentrations (41). It is important to point out that our previous data suggest that agonists acting on either imidazoline or α 2 -adrenoceptors will have the same effects on autophagy.…”

Section: Discussionmentioning

confidence: 99%

Rilmenidine attenuates toxicity of polyglutamine expansions in a mouse model of Huntington's disease

Rose¹,

Menzies²,

Renna³

et al. 2010

Human Molecular Genetics

196

144

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Huntington's disease (HD) is an autosomal dominant neurodegenerative disease caused by a polyglutamine expansion in huntingtin. There are no treatments that are known to slow the neurodegeneration caused by this mutation. Mutant huntingtin causes disease via a toxic gain-of-function mechanism and has the propensity to aggregate and form intraneuronal inclusions. One therapeutic approach for HD is to enhance the degradation of the mutant protein. We have shown that this can be achieved by upregulating autophagy, using the drug rapamycin. In order to find safer ways of inducing autophagy for clinical purposes, we previously screened United States Food and Drug Administration-approved drugs for their autophagy-stimulating potential. This screen suggested that rilmenidine, a well tolerated, safe, centrally acting anti-hypertensive drug, could induce autophagy in cell culture via a pathway that was independent of the mammalian target of rapamycin. Here we have shown that rilmenidine induces autophagy in mice and in primary neuronal culture. Rilmenidine administration attenuated the signs of disease in a HD mouse model and reduced levels of the mutant huntingtin fragment. As rilmenidine has a long safety record and is designed for chronic use, our data suggests that it should be considered for the treatment of HD and related conditions.

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“…Rilmenidine (S3341), an oxazoline, is a centrallyacting antihypertensive agent (Laubie et al, 1985;Van Zwieten et al, 1986;Koenig-BCrard et al, 1988). Specific imidazoline binding sites, probably of the subtype 1. mediate these hypotensive effects (Bouquet et al, 1989;Feldman et al, 1990;Gomez et al, 1991;Dontenwill et al, 1994;Sannajust and Head, 1994).…”

Section: Introductionmentioning

confidence: 99%

Rilmenidine activates postjunctional alpha₁‐ and alpha₂‐adrenoceptors in the canine saphenous vein

Marsault

Taddei

Boulanger

et al. 1996

Fundamemntal Clinical Pharma

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Experiments were performed to determine the subtypes of alpha-adrenoceptors involved in the contraction induced by rilmenidine in isolated canine cutaneous veins. Rings of saphenous vein (without endothelium) were suspended for the recording of isometric force in physiological salt solution. All experiments were performed in the presence of propranolol (to antagonize beta-adrenoceptors), cocaine (to inhibit neuronal uptake) and hydrocortisone (to inhibit extraneuronal uptake). In the presence of rauwolscine (an alpha 2-adrenergic blocker), rilmenidine caused concentration-dependent contractions which were inhibited by prazosin (nonselective alpha 1-antagonist) and by (+)niguldipine (selective alpha 1A-adrenergic antagonist), but not by (-)niguldipine. After treatment with phenoxybenzamine (to alkylate alpha 1-adrenoceptors), rilmenidine evoked contractions of the canine saphenous vein which were antagonized competitively by rauwolscine. The combination of rauwolscine and prazosin did not abolish contractions evoked by the highest concentrations of rilmenidine. Although binding experiments using 3H-idazoxan suggested the existence of a nonadrenergic binding site (around 20% of the total binding), contractile studies failed to demonstrate their involvement in the increases in tension evoked by rilmenidine. These experiments suggest that the contractions evoked by rilmenidine in isolated canine veins are mediated by both alpha 1A- and alpha 2-adrenoceptors.

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Cardiovascular and central nervous system effects of rilmenidine (S 3341) in rats

Cited by 43 publications

References 28 publications

Central imidazoline (I1) receptors as targets of centrally acting antihypertensives

Central imidazoline (I1) receptors as targets of centrally acting antihypertensives

Rilmenidine attenuates toxicity of polyglutamine expansions in a mouse model of Huntington's disease

Rilmenidine activates postjunctional alpha₁‐ and alpha₂‐adrenoceptors in the canine saphenous vein

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Cardiovascular and central nervous system effects of rilmenidine (S 3341) in rats

Cited by 43 publications

References 28 publications

Central imidazoline (I1) receptors as targets of centrally acting antihypertensives

Central imidazoline (I1) receptors as targets of centrally acting antihypertensives

Rilmenidine attenuates toxicity of polyglutamine expansions in a mouse model of Huntington's disease

Rilmenidine activates postjunctional alpha1‐ and alpha2‐adrenoceptors in the canine saphenous vein

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Rilmenidine activates postjunctional alpha₁‐ and alpha₂‐adrenoceptors in the canine saphenous vein