Central cardiovascular actions of agmatine, a putative clonidine-displacing substance, in conscious rabbits
Identifieur interne : 006A64 ( PascalFrancis/Corpus ); précédent : 006A63; suivant : 006A65Central cardiovascular actions of agmatine, a putative clonidine-displacing substance, in conscious rabbits
Auteurs : G. A. Head ; C. K. S. Chan ; S. J. GodwinSource :
- Neurochemistry international [ 0197-0186 ] ; 1997.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Agmatine, an endogenous clonidine-displacing substance, has been shown to have an affinity for both α2-adrenoceptors and imidazoline receptors (IR). In conscious rabbits, we have examined the cardiovascular effects of agmatine and its interaction with clonidine, a presumed agonist and 2-methoxyidazoxan, an antagonist at α2-adrenoceptors. We have also examined the effect of agmatine on agents having high affinity for I1-imidazoline receptors namely moxonidine (agonist) and efaroxan (antagonist). Initial dose-response studies showed that agmatine administered in low doses (0.01 10 μg/kg) into the fourth ventricle did not change mean arterial pressure but did produce a dose-dependent bradycardia (maximum -16±3 beats/min). A higher dose of 100 μg/kg produced an adverse reaction in the conscious animals accompanied by a marked increase in mean arterial pressure and a reversal of the bradycardia. This is in contrast to the effects of fourth ventricular clonidine and moxonidine, which caused a dose-dependent fall in both mean arterial pressure and heart rate. Agmatine when administered at the highest well-tolerated dose of 10 μg/kg did not further alter the clonidine-induced hypotension but produced a greater bradycardia (-12±4 beats/min clonidine; -29±4 beats/min clonidine plus agmatine; p<0.05). Similarly, the hypotension induced by moxonidine was not altered by agmatine but heart rate was reduced after the addition of agmatine (p<0.01). Efaroxan and 2-methoxy-idazoxan, at doses which produced no effects when given alone, similarly reversed the fall in heart rate elicited by agmatine and caused a small but significant rise in mean arterial pressure. We have previously shown that the doses of these antagonists used in this study produce an equal reversal of the bradycardia induced by fourth ventricular α-methyldopa (α2-adrenoceptor agonist) and clonidine and hence have similar α2-adrenoceptor blocking effects. Our results show that agmatine produces bradycardia as does moxonidine and clonidine but does not mimic or block the hypotensive responses to these agents. These findings do not support the hypothesis that agmatine is an endogenous ligand for IR. However, the bradycardia induced by agmatine may be mediated via α2-adrenoceptors since it was equally blocked by efaroxan and 2-methoxy-idazoxan. Thus while α2-adrenoceptor actions of agmatine on heart rate are evident at relatively low doses, the reason for the lack of α2-adrenoceptor mediated hypotension is not known.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
pA |
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Format Inist (serveur)
NO : | PASCAL 97-0164161 INIST |
---|---|
ET : | Central cardiovascular actions of agmatine, a putative clonidine-displacing substance, in conscious rabbits |
AU : | HEAD (G. A.); CHAN (C. K. S.); GODWIN (S. J.); BOUSQUET (P.) |
AF : | Neuropharmacology Laboratory, Baker Medical Research Institute/Prahran, Victoria/Australie (1 aut., 2 aut., 3 aut.); Laboratoire de Pharmacologie Cardiovasculaire et Rénale, CNRS ERS 109, Faculté de Médecine, Université Louis Pasteur, 11, rue Humann/67000 Strasbourg/France (1 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Neurochemistry international; ISSN 0197-0186; Coden NEUIDS; Etats-Unis; Da. 1997; Vol. 30; No. 1; Pp. 37-45; Bibl. 33 ref. |
LA : | Anglais |
EA : | Agmatine, an endogenous clonidine-displacing substance, has been shown to have an affinity for both α2-adrenoceptors and imidazoline receptors (IR). In conscious rabbits, we have examined the cardiovascular effects of agmatine and its interaction with clonidine, a presumed agonist and 2-methoxyidazoxan, an antagonist at α2-adrenoceptors. We have also examined the effect of agmatine on agents having high affinity for I1-imidazoline receptors namely moxonidine (agonist) and efaroxan (antagonist). Initial dose-response studies showed that agmatine administered in low doses (0.01 10 μg/kg) into the fourth ventricle did not change mean arterial pressure but did produce a dose-dependent bradycardia (maximum -16±3 beats/min). A higher dose of 100 μg/kg produced an adverse reaction in the conscious animals accompanied by a marked increase in mean arterial pressure and a reversal of the bradycardia. This is in contrast to the effects of fourth ventricular clonidine and moxonidine, which caused a dose-dependent fall in both mean arterial pressure and heart rate. Agmatine when administered at the highest well-tolerated dose of 10 μg/kg did not further alter the clonidine-induced hypotension but produced a greater bradycardia (-12±4 beats/min clonidine; -29±4 beats/min clonidine plus agmatine; p<0.05). Similarly, the hypotension induced by moxonidine was not altered by agmatine but heart rate was reduced after the addition of agmatine (p<0.01). Efaroxan and 2-methoxy-idazoxan, at doses which produced no effects when given alone, similarly reversed the fall in heart rate elicited by agmatine and caused a small but significant rise in mean arterial pressure. We have previously shown that the doses of these antagonists used in this study produce an equal reversal of the bradycardia induced by fourth ventricular α-methyldopa (α2-adrenoceptor agonist) and clonidine and hence have similar α2-adrenoceptor blocking effects. Our results show that agmatine produces bradycardia as does moxonidine and clonidine but does not mimic or block the hypotensive responses to these agents. These findings do not support the hypothesis that agmatine is an endogenous ligand for IR. However, the bradycardia induced by agmatine may be mediated via α2-adrenoceptors since it was equally blocked by efaroxan and 2-methoxy-idazoxan. Thus while α2-adrenoceptor actions of agmatine on heart rate are evident at relatively low doses, the reason for the lack of α2-adrenoceptor mediated hypotension is not known. |
CC : | 002A25E |
FD : | Agmatine; Récepteur imidazoline; Récepteur α2-adrénergique; Pression artérielle; Rythme cardiaque; Contrôle cardiovasculaire; Encéphale; Lapin |
FG : | Système nerveux central; Hémodynamique; Lagomorpha; Mammalia; Vertebrata |
ED : | Agmatine; Imidazoline receptor; α2-Adrenergic receptor; Arterial pressure; Heart rate; Cardiovascular control; Brain (vertebrata); Rabbit |
EG : | Central nervous system; Hemodynamics; Lagomorpha; Mammalia; Vertebrata |
SD : | Agmatina; Receptor imidazolina; Receptor α2-adrenérgico; Presión arterial; Ritmo cardíaco; Control cardiovascular; Encéfalo; Conejo |
LO : | INIST-18809.354000062829180060 |
ID : | 97-0164161 |
Links to Exploration step
Pascal:97-0164161Le document en format XML
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<front><div type="abstract" xml:lang="en">Agmatine, an endogenous clonidine-displacing substance, has been shown to have an affinity for both α<sub>2</sub>
-adrenoceptors and imidazoline receptors (IR). In conscious rabbits, we have examined the cardiovascular effects of agmatine and its interaction with clonidine, a presumed agonist and 2-methoxyidazoxan, an antagonist at α<sub>2</sub>
-adrenoceptors. We have also examined the effect of agmatine on agents having high affinity for I<sub>1</sub>
-imidazoline receptors namely moxonidine (agonist) and efaroxan (antagonist). Initial dose-response studies showed that agmatine administered in low doses (0.01 10 μg/kg) into the fourth ventricle did not change mean arterial pressure but did produce a dose-dependent bradycardia (maximum -16±3 beats/min). A higher dose of 100 μg/kg produced an adverse reaction in the conscious animals accompanied by a marked increase in mean arterial pressure and a reversal of the bradycardia. This is in contrast to the effects of fourth ventricular clonidine and moxonidine, which caused a dose-dependent fall in both mean arterial pressure and heart rate. Agmatine when administered at the highest well-tolerated dose of 10 μg/kg did not further alter the clonidine-induced hypotension but produced a greater bradycardia (-12±4 beats/min clonidine; -29±4 beats/min clonidine plus agmatine; p<0.05). Similarly, the hypotension induced by moxonidine was not altered by agmatine but heart rate was reduced after the addition of agmatine (p<0.01). Efaroxan and 2-methoxy-idazoxan, at doses which produced no effects when given alone, similarly reversed the fall in heart rate elicited by agmatine and caused a small but significant rise in mean arterial pressure. We have previously shown that the doses of these antagonists used in this study produce an equal reversal of the bradycardia induced by fourth ventricular α-methyldopa (α<sub>2</sub>
-adrenoceptor agonist) and clonidine and hence have similar α<sub>2</sub>
-adrenoceptor blocking effects. Our results show that agmatine produces bradycardia as does moxonidine and clonidine but does not mimic or block the hypotensive responses to these agents. These findings do not support the hypothesis that agmatine is an endogenous ligand for IR. However, the bradycardia induced by agmatine may be mediated via α<sub>2</sub>
-adrenoceptors since it was equally blocked by efaroxan and 2-methoxy-idazoxan. Thus while α<sub>2</sub>
-adrenoceptor actions of agmatine on heart rate are evident at relatively low doses, the reason for the lack of α<sub>2</sub>
-adrenoceptor mediated hypotension is not known.</div>
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<server><NO>PASCAL 97-0164161 INIST</NO>
<ET>Central cardiovascular actions of agmatine, a putative clonidine-displacing substance, in conscious rabbits</ET>
<AU>HEAD (G. A.); CHAN (C. K. S.); GODWIN (S. J.); BOUSQUET (P.)</AU>
<AF>Neuropharmacology Laboratory, Baker Medical Research Institute/Prahran, Victoria/Australie (1 aut., 2 aut., 3 aut.); Laboratoire de Pharmacologie Cardiovasculaire et Rénale, CNRS ERS 109, Faculté de Médecine, Université Louis Pasteur, 11, rue Humann/67000 Strasbourg/France (1 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neurochemistry international; ISSN 0197-0186; Coden NEUIDS; Etats-Unis; Da. 1997; Vol. 30; No. 1; Pp. 37-45; Bibl. 33 ref.</SO>
<LA>Anglais</LA>
<EA>Agmatine, an endogenous clonidine-displacing substance, has been shown to have an affinity for both α<sub>2</sub>
-adrenoceptors and imidazoline receptors (IR). In conscious rabbits, we have examined the cardiovascular effects of agmatine and its interaction with clonidine, a presumed agonist and 2-methoxyidazoxan, an antagonist at α<sub>2</sub>
-adrenoceptors. We have also examined the effect of agmatine on agents having high affinity for I<sub>1</sub>
-imidazoline receptors namely moxonidine (agonist) and efaroxan (antagonist). Initial dose-response studies showed that agmatine administered in low doses (0.01 10 μg/kg) into the fourth ventricle did not change mean arterial pressure but did produce a dose-dependent bradycardia (maximum -16±3 beats/min). A higher dose of 100 μg/kg produced an adverse reaction in the conscious animals accompanied by a marked increase in mean arterial pressure and a reversal of the bradycardia. This is in contrast to the effects of fourth ventricular clonidine and moxonidine, which caused a dose-dependent fall in both mean arterial pressure and heart rate. Agmatine when administered at the highest well-tolerated dose of 10 μg/kg did not further alter the clonidine-induced hypotension but produced a greater bradycardia (-12±4 beats/min clonidine; -29±4 beats/min clonidine plus agmatine; p<0.05). Similarly, the hypotension induced by moxonidine was not altered by agmatine but heart rate was reduced after the addition of agmatine (p<0.01). Efaroxan and 2-methoxy-idazoxan, at doses which produced no effects when given alone, similarly reversed the fall in heart rate elicited by agmatine and caused a small but significant rise in mean arterial pressure. We have previously shown that the doses of these antagonists used in this study produce an equal reversal of the bradycardia induced by fourth ventricular α-methyldopa (α<sub>2</sub>
-adrenoceptor agonist) and clonidine and hence have similar α<sub>2</sub>
-adrenoceptor blocking effects. Our results show that agmatine produces bradycardia as does moxonidine and clonidine but does not mimic or block the hypotensive responses to these agents. These findings do not support the hypothesis that agmatine is an endogenous ligand for IR. However, the bradycardia induced by agmatine may be mediated via α<sub>2</sub>
-adrenoceptors since it was equally blocked by efaroxan and 2-methoxy-idazoxan. Thus while α<sub>2</sub>
-adrenoceptor actions of agmatine on heart rate are evident at relatively low doses, the reason for the lack of α<sub>2</sub>
-adrenoceptor mediated hypotension is not known.</EA>
<CC>002A25E</CC>
<FD>Agmatine; Récepteur imidazoline; Récepteur α2-adrénergique; Pression artérielle; Rythme cardiaque; Contrôle cardiovasculaire; Encéphale; Lapin</FD>
<FG>Système nerveux central; Hémodynamique; Lagomorpha; Mammalia; Vertebrata</FG>
<ED>Agmatine; Imidazoline receptor; α2-Adrenergic receptor; Arterial pressure; Heart rate; Cardiovascular control; Brain (vertebrata); Rabbit</ED>
<EG>Central nervous system; Hemodynamics; Lagomorpha; Mammalia; Vertebrata</EG>
<SD>Agmatina; Receptor imidazolina; Receptor α2-adrenérgico; Presión arterial; Ritmo cardíaco; Control cardiovascular; Encéfalo; Conejo</SD>
<LO>INIST-18809.354000062829180060</LO>
<ID>97-0164161</ID>
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