La maladie de Parkinson en France (serveur d'exploration)

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Adrenergic supersensitivity in Parkinsonians with orthostatic hypotension

Identifieur interne : 001487 ( Istex/Corpus ); précédent : 001486; suivant : 001488

Adrenergic supersensitivity in Parkinsonians with orthostatic hypotension

Auteurs : J. M. Senard ; P. Valet ; G. Durrieu ; M. Berlan ; M. A. Tran ; J. L. Montastruc ; A. Rascol ; P. Montastruc

Source :

RBID : ISTEX:BC9DFB38359C3E0570C44CC5E126E572C41AB6D0

English descriptors

Abstract

Abstract. The adrenergic status was studied through evaluation of platelet α2‐adrenoceptor number ([3H]‐yohimbine binding sites), plasma catecholamine levels and blood pressure response to noradrenaline infusion in three groups of subjects (1) Parkinsonians with orthostatic hypotension; (2) Parkinsonians without orthostatic hypotension; and (3) control subjects. In Parkinsonians with orthostatic hypotension, systolic and diastolic blood pressures significantly (P < 0.05) decreased from 144 pM 9 and 76 pM 6 mmHg in the lying position to 95 pM 12 and 60 pM 7 mmHg after 5 min standing. In these patients, noradrenaline plasma levels were significantly low (62 pM 11 pg ml‐1, (P < 0.05) when compared with controls (219 pM 13 pg ml‐1) whereas no difference was noticed in Parkinsonians without orthostatic hypotension (195 pM 14 pg ml‐1). The noradrenaline dose required for a 25 mmHg increase in systolic blood pressure was significantly (P < 0.01) lower in Parkinsonians with orthostatic hypotension (019 pM 0.03 μg kg‐1) when compared with Parkinsonians without orthostatic hypotension (0.86 pM 0.11 μg kg‐1) or with controls (0.68 pM 0.l μg kg‐1). Platelet x2‐adrenoceptor number was higher in Parkinsonians with orthostatic hypotension (313 pM 52 fmol mg‐1 protein) than in Parkinsonians without orthostatic hypotension (168 pM 9 fmol mg‐1 protein) or in controls (175 pM 4 fmol mg‐1 protein) with no change in Kd. This study demonstrates that in patients with Parkinson's disease, orthostatic hypotension is associated with an increase in both vascular sensitivity to noradrenaline and platelet α2‐adrenoceptor number. These observations suggest the existence of an α‐adrenergic supersensitivity in response to the low levels of plasma noradrenaline.

Url:
DOI: 10.1111/j.1365-2362.1990.tb01909.x

Links to Exploration step

ISTEX:BC9DFB38359C3E0570C44CC5E126E572C41AB6D0

Le document en format XML

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<div type="abstract">Abstract. The adrenergic status was studied through evaluation of platelet α2‐adrenoceptor number ([3H]‐yohimbine binding sites), plasma catecholamine levels and blood pressure response to noradrenaline infusion in three groups of subjects (1) Parkinsonians with orthostatic hypotension; (2) Parkinsonians without orthostatic hypotension; and (3) control subjects. In Parkinsonians with orthostatic hypotension, systolic and diastolic blood pressures significantly (P < 0.05) decreased from 144 pM 9 and 76 pM 6 mmHg in the lying position to 95 pM 12 and 60 pM 7 mmHg after 5 min standing. In these patients, noradrenaline plasma levels were significantly low (62 pM 11 pg ml‐1, (P < 0.05) when compared with controls (219 pM 13 pg ml‐1) whereas no difference was noticed in Parkinsonians without orthostatic hypotension (195 pM 14 pg ml‐1). The noradrenaline dose required for a 25 mmHg increase in systolic blood pressure was significantly (P < 0.01) lower in Parkinsonians with orthostatic hypotension (019 pM 0.03 μg kg‐1) when compared with Parkinsonians without orthostatic hypotension (0.86 pM 0.11 μg kg‐1) or with controls (0.68 pM 0.l μg kg‐1). Platelet x2‐adrenoceptor number was higher in Parkinsonians with orthostatic hypotension (313 pM 52 fmol mg‐1 protein) than in Parkinsonians without orthostatic hypotension (168 pM 9 fmol mg‐1 protein) or in controls (175 pM 4 fmol mg‐1 protein) with no change in Kd. This study demonstrates that in patients with Parkinson's disease, orthostatic hypotension is associated with an increase in both vascular sensitivity to noradrenaline and platelet α2‐adrenoceptor number. These observations suggest the existence of an α‐adrenergic supersensitivity in response to the low levels of plasma noradrenaline.</div>
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<abstract>Abstract. The adrenergic status was studied through evaluation of platelet α2‐adrenoceptor number ([3H]‐yohimbine binding sites), plasma catecholamine levels and blood pressure response to noradrenaline infusion in three groups of subjects (1) Parkinsonians with orthostatic hypotension; (2) Parkinsonians without orthostatic hypotension; and (3) control subjects. In Parkinsonians with orthostatic hypotension, systolic and diastolic blood pressures significantly (P > 0.05) decreased from 144 pM 9 and 76 pM 6 mmHg in the lying position to 95 pM 12 and 60 pM 7 mmHg after 5 min standing. In these patients, noradrenaline plasma levels were significantly low (62 pM 11 pg ml‐1, (P > 0.05) when compared with controls (219 pM 13 pg ml‐1) whereas no difference was noticed in Parkinsonians without orthostatic hypotension (195 pM 14 pg ml‐1). The noradrenaline dose required for a 25 mmHg increase in systolic blood pressure was significantly (P > 0.01) lower in Parkinsonians with orthostatic hypotension (019 pM 0.03 μg kg‐1) when compared with Parkinsonians without orthostatic hypotension (0.86 pM 0.11 μg kg‐1) or with controls (0.68 pM 0.l μg kg‐1). Platelet x2‐adrenoceptor number was higher in Parkinsonians with orthostatic hypotension (313 pM 52 fmol mg‐1 protein) than in Parkinsonians without orthostatic hypotension (168 pM 9 fmol mg‐1 protein) or in controls (175 pM 4 fmol mg‐1 protein) with no change in Kd. This study demonstrates that in patients with Parkinson's disease, orthostatic hypotension is associated with an increase in both vascular sensitivity to noradrenaline and platelet α2‐adrenoceptor number. These observations suggest the existence of an α‐adrenergic supersensitivity in response to the low levels of plasma noradrenaline.</abstract>
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The adrenergic status was studied through evaluation of platelet α
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<sup>‐1</sup>
, (
<i>P</i>
< 0.05) when compared with controls (219 pM 13 pg ml
<sup>‐1</sup>
) whereas no difference was noticed in Parkinsonians without orthostatic hypotension (195 pM 14 pg ml
<sup>‐1</sup>
). The noradrenaline dose required for a 25 mmHg increase in systolic blood pressure was significantly (
<i>P</i>
< 0.01) lower in Parkinsonians with orthostatic hypotension (019 pM 0.03 μg kg
<sup>‐1</sup>
) when compared with Parkinsonians without orthostatic hypotension (0.86 pM 0.11 μg kg
<sup>‐1</sup>
) or with controls (0.68 pM 0.l μg kg
<sup>‐1</sup>
). Platelet
<i>x</i>
<sub>2</sub>
‐adrenoceptor number was higher in Parkinsonians with orthostatic hypotension (313 pM 52 fmol mg
<sup>‐1</sup>
protein) than in Parkinsonians without orthostatic hypotension (168 pM 9 fmol mg
<sup>‐1</sup>
protein) or in controls (175 pM 4 fmol mg
<sup>‐1</sup>
protein) with no change in
<i>K</i>
<sub>d</sub>
. This study demonstrates that in patients with Parkinson's disease, orthostatic hypotension is associated with an increase in both vascular sensitivity to noradrenaline and platelet α
<sub>2</sub>
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<title>Adrenergic supersensitivity in Parkinsonians with orthostatic hypotension</title>
</titleInfo>
<name type="personal">
<namePart type="given">J. M.</namePart>
<namePart type="family">SENARD</namePart>
<affiliation>Laboratoire de Pharmacologie Medicale et Clinique, Faculte de Medicine, Centre Hospitalier Universitaire, Toulouse</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">P.</namePart>
<namePart type="family">VALET</namePart>
<affiliation>Laboratoire de Pharmacologie Medicale et Clinique, Faculte de Medicine, Centre Hospitalier Universitaire, Toulouse</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">G.</namePart>
<namePart type="family">DURRIEU</namePart>
<affiliation>Laboratoire de Pharmacologie Medicale et Clinique, Faculte de Medicine, Centre Hospitalier Universitaire, Toulouse</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">BERLAN</namePart>
<affiliation>Laboratoire de Pharmacologie Medicale et Clinique, Faculte de Medicine, Centre Hospitalier Universitaire, Toulouse</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">M. A.</namePart>
<namePart type="family">TRAN</namePart>
<affiliation>Laboratoire de Pharmacologie Medicale et Clinique, Faculte de Medicine, Centre Hospitalier Universitaire, Toulouse</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J. L.</namePart>
<namePart type="family">MONTASTRUC</namePart>
<affiliation>Laboratoire de Pharmacologie Medicale et Clinique, Faculte de Medicine, Centre Hospitalier Universitaire, Toulouse</affiliation>
<affiliation>Laboratoire de Pharmacologie Medicale et Clinique, Inserm U3I7. Faculte de Medicine, Centre Hospitalier Universitaire. 37 Allees Jules Guesde, 31073 Toulouse. CEDEX, France.</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">A.</namePart>
<namePart type="family">RASCOL</namePart>
<affiliation>*Service de Neurologie, Centre Hospitalier Universitaire Purpan, Toulouse, France</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">P.</namePart>
<namePart type="family">MONTASTRUC</namePart>
<affiliation>Laboratoire de Pharmacologie Medicale et Clinique, Faculte de Medicine, Centre Hospitalier Universitaire, Toulouse</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
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<originInfo>
<publisher>Blackwell Publishing Ltd</publisher>
<place>
<placeTerm type="text">Oxford, UK</placeTerm>
</place>
<dateIssued encoding="w3cdtf">1990-12</dateIssued>
<edition>Received 15 June 1989 and in revised form 19 April 1990</edition>
<copyrightDate encoding="w3cdtf">1990</copyrightDate>
</originInfo>
<language>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
</language>
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<extent unit="references">24</extent>
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<abstract>Abstract. The adrenergic status was studied through evaluation of platelet α2‐adrenoceptor number ([3H]‐yohimbine binding sites), plasma catecholamine levels and blood pressure response to noradrenaline infusion in three groups of subjects (1) Parkinsonians with orthostatic hypotension; (2) Parkinsonians without orthostatic hypotension; and (3) control subjects. In Parkinsonians with orthostatic hypotension, systolic and diastolic blood pressures significantly (P < 0.05) decreased from 144 pM 9 and 76 pM 6 mmHg in the lying position to 95 pM 12 and 60 pM 7 mmHg after 5 min standing. In these patients, noradrenaline plasma levels were significantly low (62 pM 11 pg ml‐1, (P < 0.05) when compared with controls (219 pM 13 pg ml‐1) whereas no difference was noticed in Parkinsonians without orthostatic hypotension (195 pM 14 pg ml‐1). The noradrenaline dose required for a 25 mmHg increase in systolic blood pressure was significantly (P < 0.01) lower in Parkinsonians with orthostatic hypotension (019 pM 0.03 μg kg‐1) when compared with Parkinsonians without orthostatic hypotension (0.86 pM 0.11 μg kg‐1) or with controls (0.68 pM 0.l μg kg‐1). Platelet x2‐adrenoceptor number was higher in Parkinsonians with orthostatic hypotension (313 pM 52 fmol mg‐1 protein) than in Parkinsonians without orthostatic hypotension (168 pM 9 fmol mg‐1 protein) or in controls (175 pM 4 fmol mg‐1 protein) with no change in Kd. This study demonstrates that in patients with Parkinson's disease, orthostatic hypotension is associated with an increase in both vascular sensitivity to noradrenaline and platelet α2‐adrenoceptor number. These observations suggest the existence of an α‐adrenergic supersensitivity in response to the low levels of plasma noradrenaline.</abstract>
<subject lang="en">
<genre>keywords</genre>
<topic>α2‐adrenoceptors</topic>
<topic>orthostatic hypotension</topic>
<topic>Parkinson's disease</topic>
<topic>plasma catecholamines</topic>
<topic>platelet</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>European Journal of Clinical Investigation</title>
</titleInfo>
<genre type="journal">journal</genre>
<identifier type="ISSN">0014-2972</identifier>
<identifier type="eISSN">1365-2362</identifier>
<identifier type="DOI">10.1111/(ISSN)1365-2362</identifier>
<identifier type="PublisherID">ECI</identifier>
<part>
<date>1990</date>
<detail type="volume">
<caption>vol.</caption>
<number>20</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>6</number>
</detail>
<extent unit="pages">
<start>613</start>
<end>619</end>
<total>7</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">BC9DFB38359C3E0570C44CC5E126E572C41AB6D0</identifier>
<identifier type="DOI">10.1111/j.1365-2362.1990.tb01909.x</identifier>
<identifier type="ArticleID">ECI613</identifier>
<recordInfo>
<recordContentSource>WILEY</recordContentSource>
<recordOrigin>Blackwell Publishing Ltd</recordOrigin>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
</record>

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