Role of imidazoline receptors in cardiovascular regulation

Dontenwill, Monique; Tibiriçá, Eduardo; Greney, Hugues; Bennai, Fatima; Feldman, Josiane; Stutzmann, J; Bricca, Giampiero; Belcourt, A.; Bousquet, Pascal

doi:10.1016/0002-9149(94)90035-3

Cited by 4 publications

(3 citation statements)

References 22 publications

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“…At concentrations higher than 10-5 M, rilmenidine caused contractions which are resistant to alpha-adrenergic blockade and therefore are not likely to be mediated by activation of alpha-adrenoceptors. In the central nervous system, rilmenidine acts through the activation of imidazolinepreferring sites (Bousquet et al, 1989;Dontenwill et al, 1994). It is possible that the contraction induced by rilmenidine after adrenergic blockade is mediated by such imidazoline receptors.…”

Section: Discussionmentioning

confidence: 99%

“…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). although the involvement of alph%adrenoceptors has also been described (Urban et al 1994;Nunes.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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“…Moxonidine is a mixed I 1 -and ␣ 2 -adrenergic receptor agonist with 100-fold selectivity for I 1 over ␣ 2 -receptors (12). The selective in vivo activation of imidazoline receptors by moxonidine has been reported to cause diuresis and natriuresis as well as to stimulate plasma atrial natriuretic peptide (ANP) and urinary cGMP excretion (8,16). Renal actions of moxonidine are blocked by efaroxan (a selective I 1 -imidazoline antagonist) and partially blocked by yohimbine (an ␣ 2 -adrenoceptor antagonist).…”

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confidence: 99%

Augmentation of moxonidine-induced increase in ANP release by atrial hypertrophy

Cao¹,

Kang²,

Kim³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Imidazoline receptors are divided into I(1) and I(2) subtypes. I(1)-imidazoline receptors are distributed in the heart and are upregulated during hypertension or heart failure. The aim of this study was to define the possible role of I(1)-imidazoline receptors in the regulation of atrial natriuretic peptide (ANP) release in hypertrophied atria. Experiments were performed on isolated, perfused, hypertrophied atria from remnant-kidney hypertensive rats. The relatively selective I(1)-imidazoline receptor agonist moxonidine caused a decrease in pulse pressure. Moxonidine (3, 10, and 30 micromol/l) also caused dose-dependent increases in ANP secretion, but clonidine (an alpha(2)-adrenoceptor agonist) did not. Pretreatment with efaroxan (a selective I(1)-imidazoline receptor antagonist) or rauwolscine (a selective alpha(2)-adrenoceptor antagonist) inhibited the moxonidine-induced increases in ANP secretion and interstitial ANP concentration and decrease in pulse pressure. However, the antagonistic effect of efaroxan on moxonidine-induced ANP secretion was greater than that of rauwolscine. Neither efaroxan nor rauwolscine alone has any significant effects on ANP secretion and pulse pressure. In hypertrophied atria, the moxonidine-induced increase in ANP secretion and decrease in pulse pressure were markedly augmented compared with nonhypertrophied atria, and the relative change in ANP secretion by moxonidine was positively correlated to atrial hypertrophy. The accentuation by moxonidine of ANP secretion was attenuated by efaroxan but not by rauwolscine. These results show that moxonidine increases ANP release through (preferentially) the activation of atrial I(1)-imidazoline receptors and also via different mechanisms from clonidine, and this effect is augmented in hypertrophied atria. Therefore, we suggest that cardiac I(1)-imidazoline receptors play an important role in the regulation of blood pressure.

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Imidazoline Receptor Agonist Drugs: A New Approach to the Treatment of Systemic Hypertension

Yu.¹,

Frishman²

1996

The Journal of Clinical Pharma

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The imidazoline receptors have recently been discovered to be involved in central nervous system control of blood pressure (I-1 receptor) and in neuroprotection for cerebral ischemia (I-2 receptor). A new class of central-acting antihypertensive agents has been developed, the imidazoline receptor agonists (rilmenidine and moxonidine), which control blood pressure effectively without the adverse effects of sedation and mental depression that are usually associated with central-acting antihypertensives. This new generation of central-acting antihypertensive agents are highly selective for the imidazoline receptor, while having a low affinity for alpha 2-adrenergic receptors.

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Role of imidazoline receptors in cardiovascular regulation

Cited by 4 publications

References 22 publications

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

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

Augmentation of moxonidine-induced increase in ANP release by atrial hypertrophy

Imidazoline Receptor Agonist Drugs: A New Approach to the Treatment of Systemic Hypertension

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Role of imidazoline receptors in cardiovascular regulation

Cited by 4 publications

References 22 publications

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

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

Augmentation of moxonidine-induced increase in ANP release by atrial hypertrophy

Imidazoline Receptor Agonist Drugs: A New Approach to the Treatment of Systemic Hypertension

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

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