A study of dopaminergic sensitivity in Parkinson's disease: comparison in "de novo" and levodopa-treated patients.
Identifieur interne : 001521 ( PubMed/Curation ); précédent : 001520; suivant : 001522A study of dopaminergic sensitivity in Parkinson's disease: comparison in "de novo" and levodopa-treated patients.
Auteurs : M E Llau [France] ; G. Durrieu ; M A Tran ; J M Senard ; O. Rascol ; J L MontastrucSource :
- Clinical neuropharmacology [ 0362-5664 ] ; 1996.
English descriptors
- KwdEn :
- Adult, Aged, Antiparkinson Agents (therapeutic use), Apomorphine (pharmacology), Blood Pressure (drug effects), Dopamine (physiology), Epinephrine (blood), Female, Heart Rate (drug effects), Human Growth Hormone (blood), Humans, Hypothalamus (drug effects), Hypothalamus (physiopathology), Levodopa (therapeutic use), Male, Middle Aged, Norepinephrine (blood), Parkinson Disease (blood), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Peripheral Nervous System (drug effects), Peripheral Nervous System (physiopathology), Prolactin (blood), Sensitivity and Specificity.
- MESH :
- chemical , blood : Epinephrine, Human Growth Hormone, Norepinephrine, Prolactin.
- chemical , pharmacology : Apomorphine.
- chemical , physiology : Dopamine.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- blood : Parkinson Disease.
- drug effects : Blood Pressure, Heart Rate, Hypothalamus, Peripheral Nervous System.
- drug therapy : Parkinson Disease.
- physiopathology : Hypothalamus, Parkinson Disease, Peripheral Nervous System.
- Adult, Aged, Female, Humans, Male, Middle Aged, Sensitivity and Specificity.
Abstract
The present study investigates dopaminergic sensitivity in Parkinson's disease (PD) through the measurement of neuroendocrine (growth hormone: GH, prolactin: PRL) and cardiovascular (blood pressure: BP, heart rate: HR) responses to low doses of apomorphine (5 micrograms/kg s.c.) in three groups of subjects: 13 normal volunteers (controls), 19 "de novo" never-treated PD patients, and 14 levodopa-treated PD patients. Apomorphine did not change BP and HR but significantly decreased PRL plasma levels in controls as well as in the two groups of PD patients. GH plasma levels significantly increased after apomorphine. There was no significant difference in the changes in neuroendocrine (GH, PRL) parameters in the two groups of PD patients in comparison with controls. However, "de novo" patients exhibited a significantly higher number of apomorphine-induced orthostatic symptoms (7 of 19) than did controls (0 of 13) or treated PD patients (2 of 14). These results show that hypothalamic dopaminergic sensitivity (studied through GH and PRL responses to apomorphine) is normal in PD. In contrast, because apomorphine-induced orthostatic hypotension is mainly due to the stimulation of peripheral dopaminergic receptors, our study suggests a peripheral dopaminergic hypersensitivity in some "de novo" never treated (but not in treated) PD patients.
PubMed: 8889285
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Durrieu</name></author><author><name sortKey="Tran, M A" sort="Tran, M A" uniqKey="Tran M" first="M A" last="Tran">M A Tran</name></author><author><name sortKey="Senard, J M" sort="Senard, J M" uniqKey="Senard J" first="J M" last="Senard">J M Senard</name></author><author><name sortKey="Rascol, O" sort="Rascol, O" uniqKey="Rascol O" first="O" last="Rascol">O. Rascol</name></author><author><name sortKey="Montastruc, J L" sort="Montastruc, J L" uniqKey="Montastruc J" first="J L" last="Montastruc">J L Montastruc</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8889285</idno><idno type="pmid">8889285</idno><idno type="wicri:Area/PubMed/Corpus">001562</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001562</idno><idno type="wicri:Area/PubMed/Curation">001521</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001521</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A study of dopaminergic sensitivity in Parkinson's disease: comparison in "de novo" and levodopa-treated patients.</title><author><name sortKey="Llau, M E" sort="Llau, M E" uniqKey="Llau M" first="M E" last="Llau">M E Llau</name><affiliation wicri:level="1"><nlm:affiliation>Laboratorie de Pharmacologie Médicale et Clinique, INSERM U317, Faculté de Médecine, Toulouse, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratorie de Pharmacologie Médicale et Clinique, INSERM U317, Faculté de Médecine, Toulouse</wicri:regionArea></affiliation></author><author><name sortKey="Durrieu, G" sort="Durrieu, G" uniqKey="Durrieu G" first="G" last="Durrieu">G. Durrieu</name></author><author><name sortKey="Tran, M A" sort="Tran, M A" uniqKey="Tran M" first="M A" last="Tran">M A Tran</name></author><author><name sortKey="Senard, J M" sort="Senard, J M" uniqKey="Senard J" first="J M" last="Senard">J M Senard</name></author><author><name sortKey="Rascol, O" sort="Rascol, O" uniqKey="Rascol O" first="O" last="Rascol">O. Rascol</name></author><author><name sortKey="Montastruc, J L" sort="Montastruc, J L" uniqKey="Montastruc J" first="J L" last="Montastruc">J L Montastruc</name></author></analytic><series><title level="j">Clinical neuropharmacology</title><idno type="ISSN">0362-5664</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Antiparkinson Agents (therapeutic use)</term><term>Apomorphine (pharmacology)</term><term>Blood Pressure (drug effects)</term><term>Dopamine (physiology)</term><term>Epinephrine (blood)</term><term>Female</term><term>Heart Rate (drug effects)</term><term>Human Growth Hormone (blood)</term><term>Humans</term><term>Hypothalamus (drug effects)</term><term>Hypothalamus (physiopathology)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Norepinephrine (blood)</term><term>Parkinson Disease (blood)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Peripheral Nervous System (drug effects)</term><term>Peripheral Nervous System (physiopathology)</term><term>Prolactin (blood)</term><term>Sensitivity and Specificity</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Epinephrine</term><term>Human Growth Hormone</term><term>Norepinephrine</term><term>Prolactin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Apomorphine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Blood Pressure</term><term>Heart Rate</term><term>Hypothalamus</term><term>Peripheral Nervous System</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hypothalamus</term><term>Parkinson Disease</term><term>Peripheral Nervous System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Sensitivity and Specificity</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The present study investigates dopaminergic sensitivity in Parkinson's disease (PD) through the measurement of neuroendocrine (growth hormone: GH, prolactin: PRL) and cardiovascular (blood pressure: BP, heart rate: HR) responses to low doses of apomorphine (5 micrograms/kg s.c.) in three groups of subjects: 13 normal volunteers (controls), 19 "de novo" never-treated PD patients, and 14 levodopa-treated PD patients. Apomorphine did not change BP and HR but significantly decreased PRL plasma levels in controls as well as in the two groups of PD patients. GH plasma levels significantly increased after apomorphine. There was no significant difference in the changes in neuroendocrine (GH, PRL) parameters in the two groups of PD patients in comparison with controls. However, "de novo" patients exhibited a significantly higher number of apomorphine-induced orthostatic symptoms (7 of 19) than did controls (0 of 13) or treated PD patients (2 of 14). These results show that hypothalamic dopaminergic sensitivity (studied through GH and PRL responses to apomorphine) is normal in PD. In contrast, because apomorphine-induced orthostatic hypotension is mainly due to the stimulation of peripheral dopaminergic receptors, our study suggests a peripheral dopaminergic hypersensitivity in some "de novo" never treated (but not in treated) PD patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8889285</PMID><DateCreated><Year>1997</Year><Month>02</Month><Day>04</Day></DateCreated><DateCompleted><Year>1997</Year><Month>02</Month><Day>04</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0362-5664</ISSN><JournalIssue CitedMedium="Print"><Volume>19</Volume><Issue>5</Issue><PubDate><Year>1996</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Clinical neuropharmacology</Title><ISOAbbreviation>Clin Neuropharmacol</ISOAbbreviation></Journal><ArticleTitle>A study of dopaminergic sensitivity in Parkinson's disease: comparison in "de novo" and levodopa-treated patients.</ArticleTitle><Pagination><MedlinePgn>420-7</MedlinePgn></Pagination><Abstract><AbstractText>The present study investigates dopaminergic sensitivity in Parkinson's disease (PD) through the measurement of neuroendocrine (growth hormone: GH, prolactin: PRL) and cardiovascular (blood pressure: BP, heart rate: HR) responses to low doses of apomorphine (5 micrograms/kg s.c.) in three groups of subjects: 13 normal volunteers (controls), 19 "de novo" never-treated PD patients, and 14 levodopa-treated PD patients. Apomorphine did not change BP and HR but significantly decreased PRL plasma levels in controls as well as in the two groups of PD patients. GH plasma levels significantly increased after apomorphine. There was no significant difference in the changes in neuroendocrine (GH, PRL) parameters in the two groups of PD patients in comparison with controls. However, "de novo" patients exhibited a significantly higher number of apomorphine-induced orthostatic symptoms (7 of 19) than did controls (0 of 13) or treated PD patients (2 of 14). These results show that hypothalamic dopaminergic sensitivity (studied through GH and PRL responses to apomorphine) is normal in PD. In contrast, because apomorphine-induced orthostatic hypotension is mainly due to the stimulation of peripheral dopaminergic receptors, our study suggests a peripheral dopaminergic hypersensitivity in some "de novo" never treated (but not in treated) PD patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Llau</LastName><ForeName>M E</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Laboratorie de Pharmacologie Médicale et Clinique, INSERM U317, Faculté de Médecine, Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Durrieu</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Tran</LastName><ForeName>M A</ForeName><Initials>MA</Initials></Author><Author ValidYN="Y"><LastName>Senard</LastName><ForeName>J M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Rascol</LastName><ForeName>O</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Montastruc</LastName><ForeName>J L</ForeName><Initials>JL</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Neuropharmacol</MedlineTA><NlmUniqueID>7607910</NlmUniqueID><ISSNLinking>0362-5664</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>12629-01-5</RegistryNumber><NameOfSubstance UI="D019382">Human Growth Hormone</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>9002-62-4</RegistryNumber><NameOfSubstance UI="D011388">Prolactin</NameOfSubstance></Chemical><Chemical><RegistryNumber>N21FAR7B4S</RegistryNumber><NameOfSubstance UI="D001058">Apomorphine</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>X4W3ENH1CV</RegistryNumber><NameOfSubstance UI="D009638">Norepinephrine</NameOfSubstance></Chemical><Chemical><RegistryNumber>YKH834O4BH</RegistryNumber><NameOfSubstance UI="D004837">Epinephrine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson 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UI="D009638" MajorTopicYN="N">Norepinephrine</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017933" MajorTopicYN="N">Peripheral Nervous System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011388" MajorTopicYN="N">Prolactin</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012680" MajorTopicYN="N">Sensitivity and Specificity</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1996</Year><Month>10</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1996</Year><Month>10</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1996</Year><Month>10</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8889285</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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