Rilmenidine (S 3341) and the sympathoadrenal system: adrenoreceptors, plasma and adrenal catecholamines in dogs

Valet, Philippe; Tran, Marie-Antoinette; Damase‐Michel, Christine; Saint-Blanquat, G. De; Tran, L. Dang; Anglade, F.; Koenig-Berard, Elisabeth; Montastruc, Jean‐Louis

doi:10.1111/j.1474-8673.1988.tb00575.x

Cited by 21 publications

(11 citation statements)

References 15 publications

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“…: nicardipine(Damase-Michel et al, 1987), rilmenidine(Valet et al, 1988b), pinacidil), verapamil (Damase-Michel et al, 1989b, and quinpirole (Damase-…”

mentioning

confidence: 99%

Clonidine but not propranolol decreases plasma neuropeptide Y (NPY) levels

Damase‐Michel

Valet

et al. 1991

Fundamemntal Clinical Pharma

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The effects of acute administration of two antihypertensive drugs, clonidine and propranolol, on plasma NPY and catecholamine levels were compared in sinoaortic denervated (a model associated with a marked increase in sympathetic tone and a rise in blood pressure) and normal conscious dogs. Clonidine decreased plasma noradrenaline and NPY concentrations in both groups of animals. Propranolol failed to change plasma noradrenaline and NPY levels in sinoaortic denervated dogs but elicited a decrease in plasma noradrenaline with no change in NPY levels in normotensive animals. The present experiments show that changes in plasma noradrenaline and NPY concentrations are not always simultaneous. The decrease in plasma NPY concentrations could contribute to the sympatholytic effect of clonidine.

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“…: nicardipine(Damase-Michel et al, 1987), rilmenidine(Valet et al, 1988b), pinacidil), verapamil (Damase-Michel et al, 1989b, and quinpirole (Damase-…”

mentioning

confidence: 99%

Clonidine but not propranolol decreases plasma neuropeptide Y (NPY) levels

Damase‐Michel

Valet

et al. 1991

Fundamemntal Clinical Pharma

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“…By contrast, plasma aldosterone concentration (they are very low in SAD dogs (Valet et al, 1989b) were not modified by cicletanine. By contrast, plasma aldosterone concentration (they are very low in SAD dogs (Valet et al, 1989b) were not modified by cicletanine.…”

Section: Plasma Renin Activity (Pra) and Plasma Aldosterone Levels (Tmentioning

confidence: 75%

“…The antihypertensive effect appeared although no diuretic effect was observed in dogs, confirming the observations made in humans or in SHR rats (Chabrier et al, 1988) that these two properties are not necessarily linked. In fact, this model already allowed us to investigate the mechanisms of the antihypertensive effect of %agonists (Valet et al, 1988), calcium channel blockers (Damase-Michel et al, 1987, 1989b, potassium channel openers (Damase-Michel et al, 1989a) and D2-agonists (Damase-Michel et al, 1990). Since SAD-induced hypertension is associated with morphological renal lesions as soon as the first month (Orfila et al, 1990), it represents a suitable model for the preclinical study of antihypertensive drugs.…”

Section: Discussionmentioning

confidence: 99%

“…Briefly, carotid and aortic nerves were cut under chloralose anaesthesia (80 mgkg iv) during two successive procedures, one at time 0 and the second one seven weeks later. This model of chronic hypertension in dogs, already allowed us to study mechanisms of actions of several antihypertensive drugs (Damase-Michel et al, 1987, 1989a, 1989b. The effectiveness of baroreceptor denervation was checked by the fajlure of noradrenaline (0.5, I , 2 p g k g iv) and phenylephrine (0.1, 1 and 10 p g k g iv) to induce bradycardia and nitroglycerin (1, 3, 10 and 30 p g k g iv) to induce tachycardia just after SAD and verified before any experiment in SAD animals.…”

Section: Sinoaortic Denervation (Sad)mentioning

confidence: 99%

“…This model was selected since, as most of the patients with essential arterial hypertension, it is characterized by normal plasma catecholamine levels (Valet er al, 1989a ;Goldstein and Kopin, 1990) and low urinary kallikrein activity (Carretero and Sicli, 1989;Margolius, 1989;Valet et al, 1989b). This model was selected since, as most of the patients with essential arterial hypertension, it is characterized by normal plasma catecholamine levels (Valet er al, 1989a ;Goldstein and Kopin, 1990) and low urinary kallikrein activity (Carretero and Sicli, 1989;Margolius, 1989;Valet et al, 1989b).…”

Section: Introductionmentioning

confidence: 99%

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Effects of cicletanine on vasoactive systems in conscious sinoaortic‐denervated dogs

Damase‐Michel

Bascands

et al. 1991

Fundamemntal Clinical Pharma

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The present study investigates the antihypertensive action of cicletanine, a new antihypertensive compound with diuretic properties (or placebo), on vasopressor (catecholamines, renin-aldosterone) as well as vasodepressor (prostaglandins, kallikrein-kinin) systems in conscious chronic sinoaortic denervated (SAD) dogs. Cicletanine (10 mg/kg twice a day, per os, for one month) lowered blood pressure and heart rate. The antihypertensive action does not involve an effect on sympathetic tone (since plasma catecholamine levels were unmodified) or on plasma aldosterone levels. By contrast, urinary 6 keto PGF1 or PGE2 levels and kallikrein activity were enhanced. This result indicates that the antihypertensive effect of cicletanine is associated with a stimulation of potential vasodepressor systems (such as prostaglandins or kinins).

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Sympathoinhibition by rilmenidine in conscious rabbits: involvement of ?2-adrenoceptors

Szabó

Urban

Starke

1993

Naunyn-Schmiedeberg's Arch Pharmacol

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Cardiovascular and sympathetic nervous system effects of the mixed alpha 2-adrenoceptor and imidazoline receptor agonist rilmenidine were studied in conscious rabbits chronically instrumented for the recording of the firing rate of renal sympathetic fibers. Separate experiments were carried out on pithed rabbits with electrically stimulated (2 Hz) sympathetic outflow. Drugs were administered intravenously in a cumulative manner. In conscious rabbits, rilmenidine 0.1, 0.3 and 1.0 mg kg-1 dose-dependently lowered blood pressure, renal sympathetic nerve activity, heart rate and the plasma concentration of noradrenaline and adrenaline. The effect on blood pressure and plasma catecholamines was maximal after 0.3 mg kg-1 whereas heart rate and renal sympathetic nerve activity decreased further after rilmenidine 1.0 mg kg-1. Yohimbine 0.1 and 0.5 mg kg-1, when injected subsequently, attenuated and at the higher dose abolished all effects of rilmenidine. The effects of rilmenidine were also antagonized by the alpha 2-adrenoceptor antagonist 2-(2,3-dihydro-2-methoxy-1,4-benzodioxin-2-yl)-4,5-dihydro-1H-imid azole HCl (RX821002; 0.1 and 0.5 mg kg-1). Yohimbine 0.1 and 0.5 mg kg-1 did not attenuate or attenuated only slightly the decrease of heart rate and renal sympathetic nerve activity produced by infusion of vasopressin. In pithed rabbits with electrically-stimulated sympathetic outflow, yohimbine 0.1 submaximally and yohimbine 0.5 mg kg-1 maximally increased the plasma noradrenaline concentration. The experiments show by direct measurement of sympathetic nerve firing and plasma catecholamines that rilmenidine causes sympathoinhibition in conscious rabbits, presumably through central sites of action.(ABSTRACT TRUNCATED AT 250 WORDS)

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Rilmenidine (S 3341) and the sympathoadrenal system: adrenoreceptors, plasma and adrenal catecholamines in dogs

Cited by 21 publications

References 15 publications

Clonidine but not propranolol decreases plasma neuropeptide Y (NPY) levels

Clonidine but not propranolol decreases plasma neuropeptide Y (NPY) levels

Effects of cicletanine on vasoactive systems in conscious sinoaortic‐denervated dogs

Sympathoinhibition by rilmenidine in conscious rabbits: involvement of ?2-adrenoceptors

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