Oral fluoxetine treatment changes serotonergic sympatho-regulation in experimental type 1 diabetes
This study investigated whether fluoxetine treatment changes the 5-HT regulation on vascular sympathetic neurotransmission in type 1 diabetes. Four-week diabetes was obtained by a single alloxan s.c. administration in male Wistar rats, administering fluoxetine for 14 days (10 mg/kg/day; p.o.). Systo...
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| Veröffentlicht in: | Life sciences (1973) 2022-03, Vol.293, p.120335-120335, Article 120335 |
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| creator | García-Pedraza, José Ángel Fernández-González, Juan Francisco López, Cristina Martín, María Luisa Alarcón-Torrecillas, Claudia Rodríguez-Barbero, Alicia Morán, Asunción García-Domingo, Mónica |
| description | This study investigated whether fluoxetine treatment changes the 5-HT regulation on vascular sympathetic neurotransmission in type 1 diabetes.
Four-week diabetes was obtained by a single alloxan s.c. administration in male Wistar rats, administering fluoxetine for 14 days (10 mg/kg/day; p.o.). Systolic blood pressure, heart rate, glycaemia, body weight (BW) evolution, creatinine, and blood urea nitrogen (BUN) were monitored. Afterward, rats were pithed to perform the vascular sympathetic stimulation. 5-HT1A/1D/2A receptors expression was analysed by Western blot in thoracic aorta. Both i.v. norepinephrine and the electrical stimulation of the spinal sympathetic drive evoked vasoconstrictor responses.
Fluoxetine treatment significantly reduced the BW gain, hyperglycaemia, creatinine, and BUN in diabetic rats. The electrical-produced vasopressor responses were greater in untreated than in fluoxetine-treated diabetic rats. 5-HT decreased the sympathetic-produced vasopressor responses. While 5-CT, 8-OH-DPAT and L-694,247 (5-HT1/7, 5-HT1A and 5-HT1D agonists, respectively) reproduced 5-HT-evoked inhibition, the 5-HT2 activation by α-methyl-5-HT augmented the vasoconstrictions. The 5-CT sympatho-inhibition was reversed by 5-HT1A plus 5-HT1D antagonists (WAY-100,635 and LY310762, respectively), whereas ritanserin (5-HT2A antagonist) blocked the α-methyl-5-HT potentiating effect. Norepinephrine-generated vasoconstrictions were increased or diminished by α-methyl-5-HT or 5-CT, respectively. 5-HT1A/1D/2A receptors were expressed at vascular level, being 5-HT1A expression increased by fluoxetine in diabetic rats.
Our findings suggest that fluoxetine improves metabolic and renal profiles, changes the vasopressor responses, and 5-HT receptors modulating sympathetic activity in diabetic rats: 5-HT1A/1D are involved in the sympatho-inhibition, while 5-HT2A is implicated in the sympatho-potentiation, being both effects pre and/or postjunctional in nature.
[Display omitted]
•Fluoxetine decreases vascular noradrenergic outflow in type 1 diabetic rats.•The 5-HT vascular sympatho-regulation is changed by fluoxetine in diabetic rats.•Pre and/or postjunctional 5-HT1A and 5-HT1D are responsible of sympatho-inhibition.•Pre and/or postjunctional 5-HT2A are involved in sympatho-excitation. |
| doi_str_mv | 10.1016/j.lfs.2022.120335 |
| format | Article |
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Four-week diabetes was obtained by a single alloxan s.c. administration in male Wistar rats, administering fluoxetine for 14 days (10 mg/kg/day; p.o.). Systolic blood pressure, heart rate, glycaemia, body weight (BW) evolution, creatinine, and blood urea nitrogen (BUN) were monitored. Afterward, rats were pithed to perform the vascular sympathetic stimulation. 5-HT1A/1D/2A receptors expression was analysed by Western blot in thoracic aorta. Both i.v. norepinephrine and the electrical stimulation of the spinal sympathetic drive evoked vasoconstrictor responses.
Fluoxetine treatment significantly reduced the BW gain, hyperglycaemia, creatinine, and BUN in diabetic rats. The electrical-produced vasopressor responses were greater in untreated than in fluoxetine-treated diabetic rats. 5-HT decreased the sympathetic-produced vasopressor responses. While 5-CT, 8-OH-DPAT and L-694,247 (5-HT1/7, 5-HT1A and 5-HT1D agonists, respectively) reproduced 5-HT-evoked inhibition, the 5-HT2 activation by α-methyl-5-HT augmented the vasoconstrictions. The 5-CT sympatho-inhibition was reversed by 5-HT1A plus 5-HT1D antagonists (WAY-100,635 and LY310762, respectively), whereas ritanserin (5-HT2A antagonist) blocked the α-methyl-5-HT potentiating effect. Norepinephrine-generated vasoconstrictions were increased or diminished by α-methyl-5-HT or 5-CT, respectively. 5-HT1A/1D/2A receptors were expressed at vascular level, being 5-HT1A expression increased by fluoxetine in diabetic rats.
Our findings suggest that fluoxetine improves metabolic and renal profiles, changes the vasopressor responses, and 5-HT receptors modulating sympathetic activity in diabetic rats: 5-HT1A/1D are involved in the sympatho-inhibition, while 5-HT2A is implicated in the sympatho-potentiation, being both effects pre and/or postjunctional in nature.
[Display omitted]
•Fluoxetine decreases vascular noradrenergic outflow in type 1 diabetic rats.•The 5-HT vascular sympatho-regulation is changed by fluoxetine in diabetic rats.•Pre and/or postjunctional 5-HT1A and 5-HT1D are responsible of sympatho-inhibition.•Pre and/or postjunctional 5-HT2A are involved in sympatho-excitation.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2022.120335</identifier><identifier>PMID: 35051421</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>5-HT ; 8-Hydroxy-2-(di-n-propylamino)tetralin ; Administration, Oral ; Alloxan ; Animals ; Antagonists ; Aorta ; Blood glucose ; Blood pressure ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Body weight ; Creatinine ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (insulin dependent) ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Type 1 - drug therapy ; Diabetes Mellitus, Type 1 - metabolism ; Electrical stimuli ; Fluoxetine ; Fluoxetine - administration & dosage ; Heart rate ; Hyperglycemia ; Male ; Neurotransmission ; Norepinephrine ; Potentiation ; Rats ; Rats, Wistar ; Receptors ; Receptors, Serotonin - metabolism ; Rodents ; Serotonin - metabolism ; Serotonin Antagonists - pharmacology ; Serotonin S1 receptors ; Serotonin S2 receptors ; Serotonin Uptake Inhibitors - administration & dosage ; Stimulation ; Sympathetic neurotransmission ; Thorax ; Urea ; Vascular tone</subject><ispartof>Life sciences (1973), 2022-03, Vol.293, p.120335-120335, Article 120335</ispartof><rights>2022 The Authors</rights><rights>Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Mar 15, 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c424t-5eef48fb00972ec1d4f3b17bcfee7447af56b58beefa330827d0d769427d526c3</citedby><cites>FETCH-LOGICAL-c424t-5eef48fb00972ec1d4f3b17bcfee7447af56b58beefa330827d0d769427d526c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0024320522000352$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35051421$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>García-Pedraza, José Ángel</creatorcontrib><creatorcontrib>Fernández-González, Juan Francisco</creatorcontrib><creatorcontrib>López, Cristina</creatorcontrib><creatorcontrib>Martín, María Luisa</creatorcontrib><creatorcontrib>Alarcón-Torrecillas, Claudia</creatorcontrib><creatorcontrib>Rodríguez-Barbero, Alicia</creatorcontrib><creatorcontrib>Morán, Asunción</creatorcontrib><creatorcontrib>García-Domingo, Mónica</creatorcontrib><title>Oral fluoxetine treatment changes serotonergic sympatho-regulation in experimental type 1 diabetes</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>This study investigated whether fluoxetine treatment changes the 5-HT regulation on vascular sympathetic neurotransmission in type 1 diabetes.
Four-week diabetes was obtained by a single alloxan s.c. administration in male Wistar rats, administering fluoxetine for 14 days (10 mg/kg/day; p.o.). Systolic blood pressure, heart rate, glycaemia, body weight (BW) evolution, creatinine, and blood urea nitrogen (BUN) were monitored. Afterward, rats were pithed to perform the vascular sympathetic stimulation. 5-HT1A/1D/2A receptors expression was analysed by Western blot in thoracic aorta. Both i.v. norepinephrine and the electrical stimulation of the spinal sympathetic drive evoked vasoconstrictor responses.
Fluoxetine treatment significantly reduced the BW gain, hyperglycaemia, creatinine, and BUN in diabetic rats. The electrical-produced vasopressor responses were greater in untreated than in fluoxetine-treated diabetic rats. 5-HT decreased the sympathetic-produced vasopressor responses. While 5-CT, 8-OH-DPAT and L-694,247 (5-HT1/7, 5-HT1A and 5-HT1D agonists, respectively) reproduced 5-HT-evoked inhibition, the 5-HT2 activation by α-methyl-5-HT augmented the vasoconstrictions. The 5-CT sympatho-inhibition was reversed by 5-HT1A plus 5-HT1D antagonists (WAY-100,635 and LY310762, respectively), whereas ritanserin (5-HT2A antagonist) blocked the α-methyl-5-HT potentiating effect. Norepinephrine-generated vasoconstrictions were increased or diminished by α-methyl-5-HT or 5-CT, respectively. 5-HT1A/1D/2A receptors were expressed at vascular level, being 5-HT1A expression increased by fluoxetine in diabetic rats.
Our findings suggest that fluoxetine improves metabolic and renal profiles, changes the vasopressor responses, and 5-HT receptors modulating sympathetic activity in diabetic rats: 5-HT1A/1D are involved in the sympatho-inhibition, while 5-HT2A is implicated in the sympatho-potentiation, being both effects pre and/or postjunctional in nature.
[Display omitted]
•Fluoxetine decreases vascular noradrenergic outflow in type 1 diabetic rats.•The 5-HT vascular sympatho-regulation is changed by fluoxetine in diabetic rats.•Pre and/or postjunctional 5-HT1A and 5-HT1D are responsible of sympatho-inhibition.•Pre and/or postjunctional 5-HT2A are involved in sympatho-excitation.</description><subject>5-HT</subject><subject>8-Hydroxy-2-(di-n-propylamino)tetralin</subject><subject>Administration, Oral</subject><subject>Alloxan</subject><subject>Animals</subject><subject>Antagonists</subject><subject>Aorta</subject><subject>Blood glucose</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Body weight</subject><subject>Creatinine</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Type 1 - drug therapy</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Electrical stimuli</subject><subject>Fluoxetine</subject><subject>Fluoxetine - administration & dosage</subject><subject>Heart rate</subject><subject>Hyperglycemia</subject><subject>Male</subject><subject>Neurotransmission</subject><subject>Norepinephrine</subject><subject>Potentiation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors</subject><subject>Receptors, Serotonin - metabolism</subject><subject>Rodents</subject><subject>Serotonin - metabolism</subject><subject>Serotonin Antagonists - pharmacology</subject><subject>Serotonin S1 receptors</subject><subject>Serotonin S2 receptors</subject><subject>Serotonin Uptake Inhibitors - administration & dosage</subject><subject>Stimulation</subject><subject>Sympathetic neurotransmission</subject><subject>Thorax</subject><subject>Urea</subject><subject>Vascular tone</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kTuPFDEQhC0E4paDH0CCLJGQzNJ-jWdFhE68pJMugdjyeNp7Xs3ag-1Bt_8er_YgICDqDr4qdVcR8prBlgHr3x-2sy9bDpxvGQch1BOyYYPeddAL9pRsALjsBAd1RV6UcgAApbR4Tq6EAsUkZxsy3mU7Uz-v6QFriEhrRluPGCt19zbusdCCOdUUMe-Do-V0XGy9T13G_TrbGlKkIVJ8WDCHs6y51dOClNEp2BErlpfkmbdzwVeP85r8-Pzp-83X7vbuy7ebj7edk1zWTiF6OfgRYKc5OjZJL0amR-cRtZTaetWPahgbZoWAgesJJt3vZFsU7524Ju8uvktOP1cs1RxDcTjPNmJai-E951wPDFRD3_6DHtKaY7uuUWIArdUAjWIXyuVUSkZvlvajzSfDwJwLMAfTCjDnAsylgKZ58-i8jkec_ir-JN6ADxcAWxS_AmZTXMDocAoZXTVTCv-x_w1qMZcm</recordid><startdate>20220315</startdate><enddate>20220315</enddate><creator>García-Pedraza, José Ángel</creator><creator>Fernández-González, Juan Francisco</creator><creator>López, Cristina</creator><creator>Martín, María Luisa</creator><creator>Alarcón-Torrecillas, Claudia</creator><creator>Rodríguez-Barbero, Alicia</creator><creator>Morán, Asunción</creator><creator>García-Domingo, Mónica</creator><general>Elsevier Inc</general><general>Elsevier BV</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20220315</creationdate><title>Oral fluoxetine treatment changes serotonergic sympatho-regulation in experimental type 1 diabetes</title><author>García-Pedraza, José Ángel ; Fernández-González, Juan Francisco ; López, Cristina ; Martín, María Luisa ; Alarcón-Torrecillas, Claudia ; Rodríguez-Barbero, Alicia ; Morán, Asunción ; García-Domingo, Mónica</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c424t-5eef48fb00972ec1d4f3b17bcfee7447af56b58beefa330827d0d769427d526c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>5-HT</topic><topic>8-Hydroxy-2-(di-n-propylamino)tetralin</topic><topic>Administration, Oral</topic><topic>Alloxan</topic><topic>Animals</topic><topic>Antagonists</topic><topic>Aorta</topic><topic>Blood glucose</topic><topic>Blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Body weight</topic><topic>Creatinine</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Type 1 - drug therapy</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Electrical stimuli</topic><topic>Fluoxetine</topic><topic>Fluoxetine - administration & dosage</topic><topic>Heart rate</topic><topic>Hyperglycemia</topic><topic>Male</topic><topic>Neurotransmission</topic><topic>Norepinephrine</topic><topic>Potentiation</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors</topic><topic>Receptors, Serotonin - metabolism</topic><topic>Rodents</topic><topic>Serotonin - metabolism</topic><topic>Serotonin Antagonists - pharmacology</topic><topic>Serotonin S1 receptors</topic><topic>Serotonin S2 receptors</topic><topic>Serotonin Uptake Inhibitors - administration & dosage</topic><topic>Stimulation</topic><topic>Sympathetic neurotransmission</topic><topic>Thorax</topic><topic>Urea</topic><topic>Vascular tone</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>García-Pedraza, José Ángel</creatorcontrib><creatorcontrib>Fernández-González, Juan Francisco</creatorcontrib><creatorcontrib>López, Cristina</creatorcontrib><creatorcontrib>Martín, María Luisa</creatorcontrib><creatorcontrib>Alarcón-Torrecillas, Claudia</creatorcontrib><creatorcontrib>Rodríguez-Barbero, Alicia</creatorcontrib><creatorcontrib>Morán, Asunción</creatorcontrib><creatorcontrib>García-Domingo, Mónica</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>García-Pedraza, José Ángel</au><au>Fernández-González, Juan Francisco</au><au>López, Cristina</au><au>Martín, María Luisa</au><au>Alarcón-Torrecillas, Claudia</au><au>Rodríguez-Barbero, Alicia</au><au>Morán, Asunción</au><au>García-Domingo, Mónica</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oral fluoxetine treatment changes serotonergic sympatho-regulation in experimental type 1 diabetes</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2022-03-15</date><risdate>2022</risdate><volume>293</volume><spage>120335</spage><epage>120335</epage><pages>120335-120335</pages><artnum>120335</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>This study investigated whether fluoxetine treatment changes the 5-HT regulation on vascular sympathetic neurotransmission in type 1 diabetes.
Four-week diabetes was obtained by a single alloxan s.c. administration in male Wistar rats, administering fluoxetine for 14 days (10 mg/kg/day; p.o.). Systolic blood pressure, heart rate, glycaemia, body weight (BW) evolution, creatinine, and blood urea nitrogen (BUN) were monitored. Afterward, rats were pithed to perform the vascular sympathetic stimulation. 5-HT1A/1D/2A receptors expression was analysed by Western blot in thoracic aorta. Both i.v. norepinephrine and the electrical stimulation of the spinal sympathetic drive evoked vasoconstrictor responses.
Fluoxetine treatment significantly reduced the BW gain, hyperglycaemia, creatinine, and BUN in diabetic rats. The electrical-produced vasopressor responses were greater in untreated than in fluoxetine-treated diabetic rats. 5-HT decreased the sympathetic-produced vasopressor responses. While 5-CT, 8-OH-DPAT and L-694,247 (5-HT1/7, 5-HT1A and 5-HT1D agonists, respectively) reproduced 5-HT-evoked inhibition, the 5-HT2 activation by α-methyl-5-HT augmented the vasoconstrictions. The 5-CT sympatho-inhibition was reversed by 5-HT1A plus 5-HT1D antagonists (WAY-100,635 and LY310762, respectively), whereas ritanserin (5-HT2A antagonist) blocked the α-methyl-5-HT potentiating effect. Norepinephrine-generated vasoconstrictions were increased or diminished by α-methyl-5-HT or 5-CT, respectively. 5-HT1A/1D/2A receptors were expressed at vascular level, being 5-HT1A expression increased by fluoxetine in diabetic rats.
Our findings suggest that fluoxetine improves metabolic and renal profiles, changes the vasopressor responses, and 5-HT receptors modulating sympathetic activity in diabetic rats: 5-HT1A/1D are involved in the sympatho-inhibition, while 5-HT2A is implicated in the sympatho-potentiation, being both effects pre and/or postjunctional in nature.
[Display omitted]
•Fluoxetine decreases vascular noradrenergic outflow in type 1 diabetic rats.•The 5-HT vascular sympatho-regulation is changed by fluoxetine in diabetic rats.•Pre and/or postjunctional 5-HT1A and 5-HT1D are responsible of sympatho-inhibition.•Pre and/or postjunctional 5-HT2A are involved in sympatho-excitation.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>35051421</pmid><doi>10.1016/j.lfs.2022.120335</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Life sciences (1973), 2022-03, Vol.293, p.120335-120335, Article 120335 |
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| subjects | 5-HT 8-Hydroxy-2-(di-n-propylamino)tetralin Administration, Oral Alloxan Animals Antagonists Aorta Blood glucose Blood pressure Blood Pressure - drug effects Blood Pressure - physiology Body weight Creatinine Diabetes Diabetes mellitus Diabetes mellitus (insulin dependent) Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Type 1 - drug therapy Diabetes Mellitus, Type 1 - metabolism Electrical stimuli Fluoxetine Fluoxetine - administration & dosage Heart rate Hyperglycemia Male Neurotransmission Norepinephrine Potentiation Rats Rats, Wistar Receptors Receptors, Serotonin - metabolism Rodents Serotonin - metabolism Serotonin Antagonists - pharmacology Serotonin S1 receptors Serotonin S2 receptors Serotonin Uptake Inhibitors - administration & dosage Stimulation Sympathetic neurotransmission Thorax Urea Vascular tone |
| title | Oral fluoxetine treatment changes serotonergic sympatho-regulation in experimental type 1 diabetes |
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