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Beta-adrenergic receptors in chronic alcoholic rat hearts
Properties of cardiac β-adrenergic receptors from chronic alcoholic and control rats were studied to determine whether alterations in the receptor contribute to the decreased responsiveness of isolated working alcoholic rat hearts to β-adrenergic stimulation. The receptors, assessed in crude membran...
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Published in: | Cardiovascular research 1982-01, Vol.16 (1), p.34-39 |
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container_title | Cardiovascular research |
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creator | SEGEL, LEIGH D MASON, DEAN T |
description | Properties of cardiac β-adrenergic receptors from chronic alcoholic and control rats were studied to determine whether alterations in the receptor contribute to the decreased responsiveness of isolated working alcoholic rat hearts to β-adrenergic stimulation. The receptors, assessed in crude membrane fractions by the binding of (−)[3H]dihydroalprenolol, did not differ significantly in either number or affinity in alcoholic rats (22.5± 1.9 fmol·mg protein−1; KD=0.49 ±0.03 nmol·litre−1; n=7) compared with control rats (25.9±1.3 fmol·mg protein−1; KD=0.55 ±0.04 nmol·litre−1; n=7). Competition experiments indicated that there was no difference in the binding affinity of (−)isoprenaline for the alcoholic and control rat heart receptors, nor in the affinity of (−)propranolol for the alcoholic and control rat heart receptors. In the presence of 5′-guanylylimidodiphosphate, the affinity of (−)isoprenaline for the receptors was decreased the same amount in the alcoholic and control rat hearts. These results suggest that the β-adrenergic subsensitivity of chronic alcoholic rat hearts is mediated by a biochemical mechanism other than a direct alteration of the β-adrenergic receptor or coupling between the receptor and adenylate cyclase. |
doi_str_mv | 10.1093/cvr/16.1.34 |
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The receptors, assessed in crude membrane fractions by the binding of (−)[3H]dihydroalprenolol, did not differ significantly in either number or affinity in alcoholic rats (22.5± 1.9 fmol·mg protein−1; KD=0.49 ±0.03 nmol·litre−1; n=7) compared with control rats (25.9±1.3 fmol·mg protein−1; KD=0.55 ±0.04 nmol·litre−1; n=7). Competition experiments indicated that there was no difference in the binding affinity of (−)isoprenaline for the alcoholic and control rat heart receptors, nor in the affinity of (−)propranolol for the alcoholic and control rat heart receptors. In the presence of 5′-guanylylimidodiphosphate, the affinity of (−)isoprenaline for the receptors was decreased the same amount in the alcoholic and control rat hearts. These results suggest that the β-adrenergic subsensitivity of chronic alcoholic rat hearts is mediated by a biochemical mechanism other than a direct alteration of the β-adrenergic receptor or coupling between the receptor and adenylate cyclase.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1093/cvr/16.1.34</identifier><identifier>PMID: 6277488</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Alcoholism - metabolism ; Animals ; beta -adrenergic ; Binding, Competitive ; ethanol ; heart ; Humans ; Isoproterenol - metabolism ; Male ; Myocardium - metabolism ; Propranolol - metabolism ; Rats ; Receptors, Adrenergic - analysis ; Receptors, Adrenergic, beta - analysis</subject><ispartof>Cardiovascular research, 1982-01, Vol.16 (1), p.34-39</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-c2f1c105f06f9022cdc403f7553ef25d683a25e813ea4195e68a7c40eed6bd723</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6277488$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SEGEL, LEIGH D</creatorcontrib><creatorcontrib>MASON, DEAN T</creatorcontrib><title>Beta-adrenergic receptors in chronic alcoholic rat hearts</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>Properties of cardiac β-adrenergic receptors from chronic alcoholic and control rats were studied to determine whether alterations in the receptor contribute to the decreased responsiveness of isolated working alcoholic rat hearts to β-adrenergic stimulation. The receptors, assessed in crude membrane fractions by the binding of (−)[3H]dihydroalprenolol, did not differ significantly in either number or affinity in alcoholic rats (22.5± 1.9 fmol·mg protein−1; KD=0.49 ±0.03 nmol·litre−1; n=7) compared with control rats (25.9±1.3 fmol·mg protein−1; KD=0.55 ±0.04 nmol·litre−1; n=7). Competition experiments indicated that there was no difference in the binding affinity of (−)isoprenaline for the alcoholic and control rat heart receptors, nor in the affinity of (−)propranolol for the alcoholic and control rat heart receptors. In the presence of 5′-guanylylimidodiphosphate, the affinity of (−)isoprenaline for the receptors was decreased the same amount in the alcoholic and control rat hearts. These results suggest that the β-adrenergic subsensitivity of chronic alcoholic rat hearts is mediated by a biochemical mechanism other than a direct alteration of the β-adrenergic receptor or coupling between the receptor and adenylate cyclase.</description><subject>Alcoholism - metabolism</subject><subject>Animals</subject><subject>beta -adrenergic</subject><subject>Binding, Competitive</subject><subject>ethanol</subject><subject>heart</subject><subject>Humans</subject><subject>Isoproterenol - metabolism</subject><subject>Male</subject><subject>Myocardium - metabolism</subject><subject>Propranolol - metabolism</subject><subject>Rats</subject><subject>Receptors, Adrenergic - analysis</subject><subject>Receptors, Adrenergic, beta - analysis</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1982</creationdate><recordtype>article</recordtype><recordid>eNo9kE1Lw0AQhhdRaq2ePAs5eZG0O_uZHLWoFSoerChelu1mYqNpUndT0X_vlpaehpnn4WV4CTkHOgSa85H78SNQQxhycUD6oKVMORPykPQppVmquOLH5CSEz7hKqUWP9BTTWmRZn-Q32NnUFh4b9B-VSzw6XHWtD0nVJG7h2yYebe3aRVtvsO2SBVrfhVNyVNo64NluDsjL3e1sPEmnT_cP4-tp6gTjXepYCQ6oLKkqc8qYK5ygvIxPciyZLFTGLZOYAUcrIJeoMqujglioeaEZH5DLbe7Kt99rDJ1ZVsFhXdsG23UwIAVnoCGKV1vR-TYEj6VZ-Wpp_Z8BajZFmViUAWXAcBHti13ser7EYu_umok83fIqdPi7x9Z_GaW5lmby9m5muX7MX5-lmfF_RdJygA</recordid><startdate>198201</startdate><enddate>198201</enddate><creator>SEGEL, LEIGH D</creator><creator>MASON, DEAN T</creator><general>Oxford University Press</general><scope>BSCLL</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>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope></search><sort><creationdate>198201</creationdate><title>Beta-adrenergic receptors in chronic alcoholic rat hearts</title><author>SEGEL, LEIGH D ; MASON, DEAN T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-c2f1c105f06f9022cdc403f7553ef25d683a25e813ea4195e68a7c40eed6bd723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1982</creationdate><topic>Alcoholism - metabolism</topic><topic>Animals</topic><topic>beta -adrenergic</topic><topic>Binding, Competitive</topic><topic>ethanol</topic><topic>heart</topic><topic>Humans</topic><topic>Isoproterenol - metabolism</topic><topic>Male</topic><topic>Myocardium - metabolism</topic><topic>Propranolol - metabolism</topic><topic>Rats</topic><topic>Receptors, Adrenergic - analysis</topic><topic>Receptors, Adrenergic, beta - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SEGEL, LEIGH D</creatorcontrib><creatorcontrib>MASON, DEAN T</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SEGEL, LEIGH D</au><au>MASON, DEAN T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Beta-adrenergic receptors in chronic alcoholic rat hearts</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>1982-01</date><risdate>1982</risdate><volume>16</volume><issue>1</issue><spage>34</spage><epage>39</epage><pages>34-39</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><abstract>Properties of cardiac β-adrenergic receptors from chronic alcoholic and control rats were studied to determine whether alterations in the receptor contribute to the decreased responsiveness of isolated working alcoholic rat hearts to β-adrenergic stimulation. The receptors, assessed in crude membrane fractions by the binding of (−)[3H]dihydroalprenolol, did not differ significantly in either number or affinity in alcoholic rats (22.5± 1.9 fmol·mg protein−1; KD=0.49 ±0.03 nmol·litre−1; n=7) compared with control rats (25.9±1.3 fmol·mg protein−1; KD=0.55 ±0.04 nmol·litre−1; n=7). Competition experiments indicated that there was no difference in the binding affinity of (−)isoprenaline for the alcoholic and control rat heart receptors, nor in the affinity of (−)propranolol for the alcoholic and control rat heart receptors. In the presence of 5′-guanylylimidodiphosphate, the affinity of (−)isoprenaline for the receptors was decreased the same amount in the alcoholic and control rat hearts. These results suggest that the β-adrenergic subsensitivity of chronic alcoholic rat hearts is mediated by a biochemical mechanism other than a direct alteration of the β-adrenergic receptor or coupling between the receptor and adenylate cyclase.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>6277488</pmid><doi>10.1093/cvr/16.1.34</doi><tpages>6</tpages></addata></record> |
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source | Oxford University Press Archive |
subjects | Alcoholism - metabolism Animals beta -adrenergic Binding, Competitive ethanol heart Humans Isoproterenol - metabolism Male Myocardium - metabolism Propranolol - metabolism Rats Receptors, Adrenergic - analysis Receptors, Adrenergic, beta - analysis |
title | Beta-adrenergic receptors in chronic alcoholic rat hearts |
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