Genetic and dietary interactions: role of angiotensin AT1a receptors in response to a high-fructose diet

Department of Pharmacology and Toxicology, Boonshoft School of Medicine of Wright State University, Dayton, Ohio Submitted 27 January 2006 ; accepted in final form 18 April 2007 The renin-angiotensin system (RAS) has been implicated in the cardiovascular complications of diabetes. We showed that a h...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2007-08, Vol.293 (2), p.H1083
Hauptverfasser: Farah, Vera, Elased, Khalid M, Morris, Mariana
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page
container_issue 2
container_start_page H1083
container_title American journal of physiology. Heart and circulatory physiology
container_volume 293
creator Farah, Vera
Elased, Khalid M
Morris, Mariana
description Department of Pharmacology and Toxicology, Boonshoft School of Medicine of Wright State University, Dayton, Ohio Submitted 27 January 2006 ; accepted in final form 18 April 2007 The renin-angiotensin system (RAS) has been implicated in the cardiovascular complications of diabetes. We showed that a high-fructose diet increases blood pressure and plasma angiotensin and impairs glucose tolerance. We investigated the role of angiotensin AT 1a receptors in the development of fructose-induced cardiovascular and metabolic dysfunction. Male angiotensin AT 1a knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were fed a standard diet or one containing 60% fructose. Fructose increased mean arterial pressure (MAP) in AT1aWT but only during the dark phase (8% increase). In AT1aKO mice, fructose unexpectedly decreased MAP, during both light and dark periods (24 and 13% decrease, respectively). Analytical methods were used to measure systolic arterial pressure (SAP) and pulse interval (PI) variability in time and frequency domains. In fructose-fed AT1aWT mice, there was an increase in SAP variance and its low-frequency (LF) domain (11 ± 3 vs. 23 ± 4 mmHg 2 , variance, and 7 ± 2 vs. 17 ± 3 mmHg 2 , LF, control vs. fructose, P < 0.004). There were no changes in SAP variance in AT1aKO mice. Depressor responses to 1 -adrenergic blockade were augmented in fructose-fed AT1a WT compared with AT1aKO mice. Fructose inhibited glucose tolerance with a greater effect in AT1aWT mice. Fructose increased plasma cholesterol in both groups ( P < 0.01) and reduced ANG II in AT1aKO mice. Results document prominent interactions between genetics and diet with data showing that in the absence of angiotensin AT 1a receptors, a fructose diet decreased blood pressure. blood pressure; heart rate; autonomic nervous system; insulin; spectral analysis; insulin resistance; diabetes Address for reprint requests and other correspondence: M. Morris, Dept. of Pharmacology and Toxicology, Wright State Univ. School of Medicine, 3640 Colonel Glenn Hwy, Dayton, OH 45435 (e-mail: mariana.morris{at}wright.edu )
doi_str_mv 10.1152/ajpheart.00106.2006
format Article
fullrecord <record><control><sourceid>pubmed_highw</sourceid><recordid>TN_cdi_pubmed_primary_17449556</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>17449556</sourcerecordid><originalsourceid>FETCH-LOGICAL-h282t-a1b18cac985ae5de90b7b7e0063929cfb707dac7f6d7f37c1c9f89fbaf8618ea3</originalsourceid><addsrcrecordid>eNp1kN1OAjEQhRujEUSfwMT0BRb6w263ekWIgAmJN3i96XanbMmy3XRLlLe3BDHeeDWZmfOdzBmEHikZU5qyidp1NSgfxoRQko0ZIdkVGsYNS2jK5TUaEp7xJKM8HaC7vt8RQlKR8Vs0oGI6lWmaDVG9hBaC1Vi1Fa4sBOWP2LYBvNLBurZ_xt41gJ2Jiq11Adretni2oQp70NAF5_sIxKbvohxwcFjh2m7rxPiDDi6OTr736MaopoeHnzpCH4vXzXyVrN-Xb_PZOqlZzkKiaElzrbTMUwVpBZKUohQQs3HJpDalIKJSWpisEoYLTbU0uTSlMnlGc1B8hJ7Ovt2h3ENVdN7uY6biEjkKJmfB6cZP66Ho6mNvXeO2x-Ly04JJXrBiRUnOI_HyP7E4NM0GvsIv-ocsusrwbwENg0g</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Genetic and dietary interactions: role of angiotensin AT1a receptors in response to a high-fructose diet</title><source>MEDLINE</source><source>American Physiological Society Paid</source><source>Elektronische Zeitschriftenbibliothek</source><source>Alma/SFX Local Collection</source><creator>Farah, Vera ; Elased, Khalid M ; Morris, Mariana</creator><creatorcontrib>Farah, Vera ; Elased, Khalid M ; Morris, Mariana</creatorcontrib><description>Department of Pharmacology and Toxicology, Boonshoft School of Medicine of Wright State University, Dayton, Ohio Submitted 27 January 2006 ; accepted in final form 18 April 2007 The renin-angiotensin system (RAS) has been implicated in the cardiovascular complications of diabetes. We showed that a high-fructose diet increases blood pressure and plasma angiotensin and impairs glucose tolerance. We investigated the role of angiotensin AT 1a receptors in the development of fructose-induced cardiovascular and metabolic dysfunction. Male angiotensin AT 1a knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were fed a standard diet or one containing 60% fructose. Fructose increased mean arterial pressure (MAP) in AT1aWT but only during the dark phase (8% increase). In AT1aKO mice, fructose unexpectedly decreased MAP, during both light and dark periods (24 and 13% decrease, respectively). Analytical methods were used to measure systolic arterial pressure (SAP) and pulse interval (PI) variability in time and frequency domains. In fructose-fed AT1aWT mice, there was an increase in SAP variance and its low-frequency (LF) domain (11 ± 3 vs. 23 ± 4 mmHg 2 , variance, and 7 ± 2 vs. 17 ± 3 mmHg 2 , LF, control vs. fructose, P &lt; 0.004). There were no changes in SAP variance in AT1aKO mice. Depressor responses to 1 -adrenergic blockade were augmented in fructose-fed AT1a WT compared with AT1aKO mice. Fructose inhibited glucose tolerance with a greater effect in AT1aWT mice. Fructose increased plasma cholesterol in both groups ( P &lt; 0.01) and reduced ANG II in AT1aKO mice. Results document prominent interactions between genetics and diet with data showing that in the absence of angiotensin AT 1a receptors, a fructose diet decreased blood pressure. blood pressure; heart rate; autonomic nervous system; insulin; spectral analysis; insulin resistance; diabetes Address for reprint requests and other correspondence: M. Morris, Dept. of Pharmacology and Toxicology, Wright State Univ. School of Medicine, 3640 Colonel Glenn Hwy, Dayton, OH 45435 (e-mail: mariana.morris{at}wright.edu )</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00106.2006</identifier><identifier>PMID: 17449556</identifier><language>eng</language><publisher>United States</publisher><subject>Adrenergic alpha-1 Receptor Antagonists ; Adrenergic alpha-Antagonists - pharmacology ; Angiotensin II - blood ; Animals ; Blood Glucose - metabolism ; Blood Pressure ; Circadian Rhythm ; Dietary Carbohydrates ; Disease Models, Animal ; Fructose ; Glucose Intolerance - blood ; Glucose Intolerance - chemically induced ; Glucose Intolerance - genetics ; Glucose Intolerance - metabolism ; Glucose Intolerance - physiopathology ; Heart Rate ; Hypertension - blood ; Hypertension - chemically induced ; Hypertension - genetics ; Hypertension - metabolism ; Hypertension - physiopathology ; Insulin Resistance - genetics ; Lipids - blood ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Prazosin - pharmacology ; Receptor, Angiotensin, Type 1 - deficiency ; Receptor, Angiotensin, Type 1 - genetics ; Receptor, Angiotensin, Type 1 - metabolism ; Receptors, Adrenergic, alpha-1 - metabolism ; Renin-Angiotensin System - genetics ; Signal Transduction - genetics ; Sympathetic Nervous System - drug effects ; Sympathetic Nervous System - metabolism ; Sympathetic Nervous System - physiopathology ; Time Factors</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2007-08, Vol.293 (2), p.H1083</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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/17449556$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Farah, Vera</creatorcontrib><creatorcontrib>Elased, Khalid M</creatorcontrib><creatorcontrib>Morris, Mariana</creatorcontrib><title>Genetic and dietary interactions: role of angiotensin AT1a receptors in response to a high-fructose diet</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Department of Pharmacology and Toxicology, Boonshoft School of Medicine of Wright State University, Dayton, Ohio Submitted 27 January 2006 ; accepted in final form 18 April 2007 The renin-angiotensin system (RAS) has been implicated in the cardiovascular complications of diabetes. We showed that a high-fructose diet increases blood pressure and plasma angiotensin and impairs glucose tolerance. We investigated the role of angiotensin AT 1a receptors in the development of fructose-induced cardiovascular and metabolic dysfunction. Male angiotensin AT 1a knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were fed a standard diet or one containing 60% fructose. Fructose increased mean arterial pressure (MAP) in AT1aWT but only during the dark phase (8% increase). In AT1aKO mice, fructose unexpectedly decreased MAP, during both light and dark periods (24 and 13% decrease, respectively). Analytical methods were used to measure systolic arterial pressure (SAP) and pulse interval (PI) variability in time and frequency domains. In fructose-fed AT1aWT mice, there was an increase in SAP variance and its low-frequency (LF) domain (11 ± 3 vs. 23 ± 4 mmHg 2 , variance, and 7 ± 2 vs. 17 ± 3 mmHg 2 , LF, control vs. fructose, P &lt; 0.004). There were no changes in SAP variance in AT1aKO mice. Depressor responses to 1 -adrenergic blockade were augmented in fructose-fed AT1a WT compared with AT1aKO mice. Fructose inhibited glucose tolerance with a greater effect in AT1aWT mice. Fructose increased plasma cholesterol in both groups ( P &lt; 0.01) and reduced ANG II in AT1aKO mice. Results document prominent interactions between genetics and diet with data showing that in the absence of angiotensin AT 1a receptors, a fructose diet decreased blood pressure. blood pressure; heart rate; autonomic nervous system; insulin; spectral analysis; insulin resistance; diabetes Address for reprint requests and other correspondence: M. Morris, Dept. of Pharmacology and Toxicology, Wright State Univ. School of Medicine, 3640 Colonel Glenn Hwy, Dayton, OH 45435 (e-mail: mariana.morris{at}wright.edu )</description><subject>Adrenergic alpha-1 Receptor Antagonists</subject><subject>Adrenergic alpha-Antagonists - pharmacology</subject><subject>Angiotensin II - blood</subject><subject>Animals</subject><subject>Blood Glucose - metabolism</subject><subject>Blood Pressure</subject><subject>Circadian Rhythm</subject><subject>Dietary Carbohydrates</subject><subject>Disease Models, Animal</subject><subject>Fructose</subject><subject>Glucose Intolerance - blood</subject><subject>Glucose Intolerance - chemically induced</subject><subject>Glucose Intolerance - genetics</subject><subject>Glucose Intolerance - metabolism</subject><subject>Glucose Intolerance - physiopathology</subject><subject>Heart Rate</subject><subject>Hypertension - blood</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - genetics</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>Insulin Resistance - genetics</subject><subject>Lipids - blood</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Prazosin - pharmacology</subject><subject>Receptor, Angiotensin, Type 1 - deficiency</subject><subject>Receptor, Angiotensin, Type 1 - genetics</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Receptors, Adrenergic, alpha-1 - metabolism</subject><subject>Renin-Angiotensin System - genetics</subject><subject>Signal Transduction - genetics</subject><subject>Sympathetic Nervous System - drug effects</subject><subject>Sympathetic Nervous System - metabolism</subject><subject>Sympathetic Nervous System - physiopathology</subject><subject>Time Factors</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kN1OAjEQhRujEUSfwMT0BRb6w263ekWIgAmJN3i96XanbMmy3XRLlLe3BDHeeDWZmfOdzBmEHikZU5qyidp1NSgfxoRQko0ZIdkVGsYNS2jK5TUaEp7xJKM8HaC7vt8RQlKR8Vs0oGI6lWmaDVG9hBaC1Vi1Fa4sBOWP2LYBvNLBurZ_xt41gJ2Jiq11Adretni2oQp70NAF5_sIxKbvohxwcFjh2m7rxPiDDi6OTr736MaopoeHnzpCH4vXzXyVrN-Xb_PZOqlZzkKiaElzrbTMUwVpBZKUohQQs3HJpDalIKJSWpisEoYLTbU0uTSlMnlGc1B8hJ7Ovt2h3ENVdN7uY6biEjkKJmfB6cZP66Ho6mNvXeO2x-Ly04JJXrBiRUnOI_HyP7E4NM0GvsIv-ocsusrwbwENg0g</recordid><startdate>20070801</startdate><enddate>20070801</enddate><creator>Farah, Vera</creator><creator>Elased, Khalid M</creator><creator>Morris, Mariana</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20070801</creationdate><title>Genetic and dietary interactions: role of angiotensin AT1a receptors in response to a high-fructose diet</title><author>Farah, Vera ; Elased, Khalid M ; Morris, Mariana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h282t-a1b18cac985ae5de90b7b7e0063929cfb707dac7f6d7f37c1c9f89fbaf8618ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adrenergic alpha-1 Receptor Antagonists</topic><topic>Adrenergic alpha-Antagonists - pharmacology</topic><topic>Angiotensin II - blood</topic><topic>Animals</topic><topic>Blood Glucose - metabolism</topic><topic>Blood Pressure</topic><topic>Circadian Rhythm</topic><topic>Dietary Carbohydrates</topic><topic>Disease Models, Animal</topic><topic>Fructose</topic><topic>Glucose Intolerance - blood</topic><topic>Glucose Intolerance - chemically induced</topic><topic>Glucose Intolerance - genetics</topic><topic>Glucose Intolerance - metabolism</topic><topic>Glucose Intolerance - physiopathology</topic><topic>Heart Rate</topic><topic>Hypertension - blood</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - genetics</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>Insulin Resistance - genetics</topic><topic>Lipids - blood</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Prazosin - pharmacology</topic><topic>Receptor, Angiotensin, Type 1 - deficiency</topic><topic>Receptor, Angiotensin, Type 1 - genetics</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Receptors, Adrenergic, alpha-1 - metabolism</topic><topic>Renin-Angiotensin System - genetics</topic><topic>Signal Transduction - genetics</topic><topic>Sympathetic Nervous System - drug effects</topic><topic>Sympathetic Nervous System - metabolism</topic><topic>Sympathetic Nervous System - physiopathology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Farah, Vera</creatorcontrib><creatorcontrib>Elased, Khalid M</creatorcontrib><creatorcontrib>Morris, Mariana</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Farah, Vera</au><au>Elased, Khalid M</au><au>Morris, Mariana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic and dietary interactions: role of angiotensin AT1a receptors in response to a high-fructose diet</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2007-08-01</date><risdate>2007</risdate><volume>293</volume><issue>2</issue><spage>H1083</spage><pages>H1083-</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Department of Pharmacology and Toxicology, Boonshoft School of Medicine of Wright State University, Dayton, Ohio Submitted 27 January 2006 ; accepted in final form 18 April 2007 The renin-angiotensin system (RAS) has been implicated in the cardiovascular complications of diabetes. We showed that a high-fructose diet increases blood pressure and plasma angiotensin and impairs glucose tolerance. We investigated the role of angiotensin AT 1a receptors in the development of fructose-induced cardiovascular and metabolic dysfunction. Male angiotensin AT 1a knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were fed a standard diet or one containing 60% fructose. Fructose increased mean arterial pressure (MAP) in AT1aWT but only during the dark phase (8% increase). In AT1aKO mice, fructose unexpectedly decreased MAP, during both light and dark periods (24 and 13% decrease, respectively). Analytical methods were used to measure systolic arterial pressure (SAP) and pulse interval (PI) variability in time and frequency domains. In fructose-fed AT1aWT mice, there was an increase in SAP variance and its low-frequency (LF) domain (11 ± 3 vs. 23 ± 4 mmHg 2 , variance, and 7 ± 2 vs. 17 ± 3 mmHg 2 , LF, control vs. fructose, P &lt; 0.004). There were no changes in SAP variance in AT1aKO mice. Depressor responses to 1 -adrenergic blockade were augmented in fructose-fed AT1a WT compared with AT1aKO mice. Fructose inhibited glucose tolerance with a greater effect in AT1aWT mice. Fructose increased plasma cholesterol in both groups ( P &lt; 0.01) and reduced ANG II in AT1aKO mice. Results document prominent interactions between genetics and diet with data showing that in the absence of angiotensin AT 1a receptors, a fructose diet decreased blood pressure. blood pressure; heart rate; autonomic nervous system; insulin; spectral analysis; insulin resistance; diabetes Address for reprint requests and other correspondence: M. Morris, Dept. of Pharmacology and Toxicology, Wright State Univ. School of Medicine, 3640 Colonel Glenn Hwy, Dayton, OH 45435 (e-mail: mariana.morris{at}wright.edu )</abstract><cop>United States</cop><pmid>17449556</pmid><doi>10.1152/ajpheart.00106.2006</doi></addata></record>
fulltext fulltext
identifier ISSN: 0363-6135
ispartof American journal of physiology. Heart and circulatory physiology, 2007-08, Vol.293 (2), p.H1083
issn 0363-6135
1522-1539
language eng
recordid cdi_pubmed_primary_17449556
source MEDLINE; American Physiological Society Paid; Elektronische Zeitschriftenbibliothek; Alma/SFX Local Collection
subjects Adrenergic alpha-1 Receptor Antagonists
Adrenergic alpha-Antagonists - pharmacology
Angiotensin II - blood
Animals
Blood Glucose - metabolism
Blood Pressure
Circadian Rhythm
Dietary Carbohydrates
Disease Models, Animal
Fructose
Glucose Intolerance - blood
Glucose Intolerance - chemically induced
Glucose Intolerance - genetics
Glucose Intolerance - metabolism
Glucose Intolerance - physiopathology
Heart Rate
Hypertension - blood
Hypertension - chemically induced
Hypertension - genetics
Hypertension - metabolism
Hypertension - physiopathology
Insulin Resistance - genetics
Lipids - blood
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Prazosin - pharmacology
Receptor, Angiotensin, Type 1 - deficiency
Receptor, Angiotensin, Type 1 - genetics
Receptor, Angiotensin, Type 1 - metabolism
Receptors, Adrenergic, alpha-1 - metabolism
Renin-Angiotensin System - genetics
Signal Transduction - genetics
Sympathetic Nervous System - drug effects
Sympathetic Nervous System - metabolism
Sympathetic Nervous System - physiopathology
Time Factors
title Genetic and dietary interactions: role of angiotensin AT1a receptors in response to a high-fructose diet
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T10%3A34%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_highw&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Genetic%20and%20dietary%20interactions:%20role%20of%20angiotensin%20AT1a%20receptors%20in%20response%20to%20a%20high-fructose%20diet&rft.jtitle=American%20journal%20of%20physiology.%20Heart%20and%20circulatory%20physiology&rft.au=Farah,%20Vera&rft.date=2007-08-01&rft.volume=293&rft.issue=2&rft.spage=H1083&rft.pages=H1083-&rft.issn=0363-6135&rft.eissn=1522-1539&rft_id=info:doi/10.1152/ajpheart.00106.2006&rft_dat=%3Cpubmed_highw%3E17449556%3C/pubmed_highw%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/17449556&rfr_iscdi=true