Synergistic interaction between enalapril, L‐arginine and tetrahydrobiopterin in smooth muscle cell apoptosis and aortic remodeling induction in SHR
Smooth muscle cell (SMC) apoptosis occurs at the onset of enalapril‐induced regression of aortic hypertrophy in SHR. A potential mechanism is the correction of endothelial dysfunction (ED) leading to reduced production of reactive oxygen species and enhanced bioavailability of nitric oxide (NO), a p...
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| creator | Sarkissian, Shant Der Marchand, Eve‐Lyne Duguay, David DeBlois, Denis |
| description | Smooth muscle cell (SMC) apoptosis occurs at the onset of enalapril‐induced regression of aortic hypertrophy in SHR. A potential mechanism is the correction of endothelial dysfunction (ED) leading to reduced production of reactive oxygen species and enhanced bioavailability of nitric oxide (NO), a potent apoptosis inducer. Stimulants of NO include the precursor L‐arginine and the NO synthase cofactor tetrahydrobiopterin (BH4), which correct ED in several models.
The objective was to examine the relationships between ED and the cell growth/death balance during vascular remodeling induced by enalapril in SHR.
SHR, 10‐week‐old, received enalapril (ENA: 30 mg.kg−1.day−1 p.o.) for 1 or 2 weeks, or a co‐treatment of L‐arginine (2.0 g.kg−1.day−1 p.o.) and BH4 (5.4 mg.kg−1.day−1 i.p. twice daily) administered alone (group: LB) or in combination with enalapril (ENA+LB) for 1 week. Controls received vehicle.
After 1 week, ED was completely corrected with LB but not affected significantly by ENA, whereas both treatments failed to induce SMC apoptosis or aortic remodeling. The correction of ED and the induction of SMC apoptosis (3.3‐fold increase in TUNEL labeling) required 2 weeks of ENA treatment. The combination of LB with ENA for 1 week, however, was additive for the reduction of SMC proliferation, and synergistic for the induction of apoptosis and regression of vascular hypertrophy. These interactions were independent of blood pressure regulation.
Our results suggest that the correction of ED is not sufficient to induce SMC apoptosis and vascular remodeling, although it facilitates these responses during enalapril treatment.
British Journal of Pharmacology (2004) 142, 912–918. doi:10.1038/sj.bjp.0705830 |
| doi_str_mv | 10.1038/sj.bjp.0705830 |
| format | Article |
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The objective was to examine the relationships between ED and the cell growth/death balance during vascular remodeling induced by enalapril in SHR.
SHR, 10‐week‐old, received enalapril (ENA: 30 mg.kg−1.day−1 p.o.) for 1 or 2 weeks, or a co‐treatment of L‐arginine (2.0 g.kg−1.day−1 p.o.) and BH4 (5.4 mg.kg−1.day−1 i.p. twice daily) administered alone (group: LB) or in combination with enalapril (ENA+LB) for 1 week. Controls received vehicle.
After 1 week, ED was completely corrected with LB but not affected significantly by ENA, whereas both treatments failed to induce SMC apoptosis or aortic remodeling. The correction of ED and the induction of SMC apoptosis (3.3‐fold increase in TUNEL labeling) required 2 weeks of ENA treatment. The combination of LB with ENA for 1 week, however, was additive for the reduction of SMC proliferation, and synergistic for the induction of apoptosis and regression of vascular hypertrophy. These interactions were independent of blood pressure regulation.
Our results suggest that the correction of ED is not sufficient to induce SMC apoptosis and vascular remodeling, although it facilitates these responses during enalapril treatment.
British Journal of Pharmacology (2004) 142, 912–918. doi:10.1038/sj.bjp.0705830</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0705830</identifier><identifier>PMID: 15197102</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acetylcholine - pharmacology ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Animals ; Aorta, Thoracic - cytology ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - physiology ; apoptosis ; Apoptosis - drug effects ; Arginine - pharmacology ; Biological and medical sciences ; Biopterins - analogs & derivatives ; Biopterins - pharmacology ; Blood Pressure - drug effects ; Body Weight - drug effects ; DNA Fragmentation - drug effects ; Drug Synergism ; enalapril ; Enalapril - pharmacology ; Endothelial dysfunction ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - pathology ; Endothelium, Vascular - physiopathology ; hypertension ; In Situ Nick-End Labeling ; Male ; Medical sciences ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - pathology ; nitric oxide ; Nitric Oxide - metabolism ; Pharmacology. Drug treatments ; Rats ; Rats, Inbred SHR ; Reactive Oxygen Species - metabolism ; tetrahydrobiopterin ; Vasodilator Agents - pharmacology</subject><ispartof>British journal of pharmacology, 2004-07, Vol.142 (5), p.912-918</ispartof><rights>2004 British Pharmacological Society</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2004</rights><rights>Copyright 2004, Nature Publishing Group 2004 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4872-835666873f1fb74c6f5a953aa1ee8dd770a21a914f9c1a8537b8ef80de8be863</citedby><cites>FETCH-LOGICAL-c4872-835666873f1fb74c6f5a953aa1ee8dd770a21a914f9c1a8537b8ef80de8be863</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1575062/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1575062/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27903,27904,45553,45554,46387,46811,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15958473$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15197102$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sarkissian, Shant Der</creatorcontrib><creatorcontrib>Marchand, Eve‐Lyne</creatorcontrib><creatorcontrib>Duguay, David</creatorcontrib><creatorcontrib>DeBlois, Denis</creatorcontrib><title>Synergistic interaction between enalapril, L‐arginine and tetrahydrobiopterin in smooth muscle cell apoptosis and aortic remodeling induction in SHR</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Smooth muscle cell (SMC) apoptosis occurs at the onset of enalapril‐induced regression of aortic hypertrophy in SHR. A potential mechanism is the correction of endothelial dysfunction (ED) leading to reduced production of reactive oxygen species and enhanced bioavailability of nitric oxide (NO), a potent apoptosis inducer. Stimulants of NO include the precursor L‐arginine and the NO synthase cofactor tetrahydrobiopterin (BH4), which correct ED in several models.
The objective was to examine the relationships between ED and the cell growth/death balance during vascular remodeling induced by enalapril in SHR.
SHR, 10‐week‐old, received enalapril (ENA: 30 mg.kg−1.day−1 p.o.) for 1 or 2 weeks, or a co‐treatment of L‐arginine (2.0 g.kg−1.day−1 p.o.) and BH4 (5.4 mg.kg−1.day−1 i.p. twice daily) administered alone (group: LB) or in combination with enalapril (ENA+LB) for 1 week. Controls received vehicle.
After 1 week, ED was completely corrected with LB but not affected significantly by ENA, whereas both treatments failed to induce SMC apoptosis or aortic remodeling. The correction of ED and the induction of SMC apoptosis (3.3‐fold increase in TUNEL labeling) required 2 weeks of ENA treatment. The combination of LB with ENA for 1 week, however, was additive for the reduction of SMC proliferation, and synergistic for the induction of apoptosis and regression of vascular hypertrophy. These interactions were independent of blood pressure regulation.
Our results suggest that the correction of ED is not sufficient to induce SMC apoptosis and vascular remodeling, although it facilitates these responses during enalapril treatment.
British Journal of Pharmacology (2004) 142, 912–918. doi:10.1038/sj.bjp.0705830</description><subject>Acetylcholine - pharmacology</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Aorta, Thoracic - cytology</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Aorta, Thoracic - physiology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Arginine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biopterins - analogs & derivatives</subject><subject>Biopterins - pharmacology</subject><subject>Blood Pressure - drug effects</subject><subject>Body Weight - drug effects</subject><subject>DNA Fragmentation - drug effects</subject><subject>Drug Synergism</subject><subject>enalapril</subject><subject>Enalapril - pharmacology</subject><subject>Endothelial dysfunction</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - pathology</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>hypertension</subject><subject>In Situ Nick-End Labeling</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>tetrahydrobiopterin</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkbGO1DAURS0EYoeFlhJZSHRksOM4dhqkZQUM0kggdnvLcV5mHDn2YCespuMTqPhAvgQvE8FSUbl4597r9y5CTylZU8LkqzSs2-GwJoJwycg9tKKVqAvOJL2PVoQQUVAq5Rl6lNJASB4K_hCdUU4bQUm5Qj-ujh7izqbJGmz9BFGbyQaPW5huADwGr50-ROte4u3Pb991Zr31gLXv8ART1PtjF0NrwyFrrc8eOI0hTHs8zsk4wAacw_qQ5yHZ9FunQ7yNizCGDpz1u6zq5lNu1l9tPj9GD3rtEjxZ3nN0_e7t9eWm2H58_-HyYluYSoqykIzXdS0F62nfisrUPdcNZ1pTANl1QhBdUt3Qqm8M1ZIz0UroJelAtiBrdo5en2wPcztCZ8DnhZzK6446HlXQVv078XavduGrolxwUpfZ4PliEMOXGdKkhjDHfLKkSipoQ1glMrQ-QSaGlCL0fwIoUbctqjSo3KJaWsyCZ3e_9RdfasvAiwXQyWjXR-2NTXe4hsscnDl24m6sg-N_YtWbT5uS8ZL9AkFFvDw</recordid><startdate>200407</startdate><enddate>200407</enddate><creator>Sarkissian, Shant Der</creator><creator>Marchand, Eve‐Lyne</creator><creator>Duguay, David</creator><creator>DeBlois, Denis</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>200407</creationdate><title>Synergistic interaction between enalapril, L‐arginine and tetrahydrobiopterin in smooth muscle cell apoptosis and aortic remodeling induction in SHR</title><author>Sarkissian, Shant Der ; Marchand, Eve‐Lyne ; Duguay, David ; DeBlois, Denis</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4872-835666873f1fb74c6f5a953aa1ee8dd770a21a914f9c1a8537b8ef80de8be863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Aorta, Thoracic - cytology</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Aorta, Thoracic - physiology</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Arginine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biopterins - analogs & derivatives</topic><topic>Biopterins - pharmacology</topic><topic>Blood Pressure - drug effects</topic><topic>Body Weight - drug effects</topic><topic>DNA Fragmentation - drug effects</topic><topic>Drug Synergism</topic><topic>enalapril</topic><topic>Enalapril - pharmacology</topic><topic>Endothelial dysfunction</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - pathology</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>hypertension</topic><topic>In Situ Nick-End Labeling</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>tetrahydrobiopterin</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sarkissian, Shant Der</creatorcontrib><creatorcontrib>Marchand, Eve‐Lyne</creatorcontrib><creatorcontrib>Duguay, David</creatorcontrib><creatorcontrib>DeBlois, Denis</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sarkissian, Shant Der</au><au>Marchand, Eve‐Lyne</au><au>Duguay, David</au><au>DeBlois, Denis</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synergistic interaction between enalapril, L‐arginine and tetrahydrobiopterin in smooth muscle cell apoptosis and aortic remodeling induction in SHR</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2004-07</date><risdate>2004</risdate><volume>142</volume><issue>5</issue><spage>912</spage><epage>918</epage><pages>912-918</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Smooth muscle cell (SMC) apoptosis occurs at the onset of enalapril‐induced regression of aortic hypertrophy in SHR. A potential mechanism is the correction of endothelial dysfunction (ED) leading to reduced production of reactive oxygen species and enhanced bioavailability of nitric oxide (NO), a potent apoptosis inducer. Stimulants of NO include the precursor L‐arginine and the NO synthase cofactor tetrahydrobiopterin (BH4), which correct ED in several models.
The objective was to examine the relationships between ED and the cell growth/death balance during vascular remodeling induced by enalapril in SHR.
SHR, 10‐week‐old, received enalapril (ENA: 30 mg.kg−1.day−1 p.o.) for 1 or 2 weeks, or a co‐treatment of L‐arginine (2.0 g.kg−1.day−1 p.o.) and BH4 (5.4 mg.kg−1.day−1 i.p. twice daily) administered alone (group: LB) or in combination with enalapril (ENA+LB) for 1 week. Controls received vehicle.
After 1 week, ED was completely corrected with LB but not affected significantly by ENA, whereas both treatments failed to induce SMC apoptosis or aortic remodeling. The correction of ED and the induction of SMC apoptosis (3.3‐fold increase in TUNEL labeling) required 2 weeks of ENA treatment. The combination of LB with ENA for 1 week, however, was additive for the reduction of SMC proliferation, and synergistic for the induction of apoptosis and regression of vascular hypertrophy. These interactions were independent of blood pressure regulation.
Our results suggest that the correction of ED is not sufficient to induce SMC apoptosis and vascular remodeling, although it facilitates these responses during enalapril treatment.
British Journal of Pharmacology (2004) 142, 912–918. doi:10.1038/sj.bjp.0705830</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>15197102</pmid><doi>10.1038/sj.bjp.0705830</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylcholine - pharmacology Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Aorta, Thoracic - cytology Aorta, Thoracic - drug effects Aorta, Thoracic - physiology apoptosis Apoptosis - drug effects Arginine - pharmacology Biological and medical sciences Biopterins - analogs & derivatives Biopterins - pharmacology Blood Pressure - drug effects Body Weight - drug effects DNA Fragmentation - drug effects Drug Synergism enalapril Enalapril - pharmacology Endothelial dysfunction Endothelium, Vascular - drug effects Endothelium, Vascular - pathology Endothelium, Vascular - physiopathology hypertension In Situ Nick-End Labeling Male Medical sciences Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - pathology nitric oxide Nitric Oxide - metabolism Pharmacology. Drug treatments Rats Rats, Inbred SHR Reactive Oxygen Species - metabolism tetrahydrobiopterin Vasodilator Agents - pharmacology |
| title | Synergistic interaction between enalapril, L‐arginine and tetrahydrobiopterin in smooth muscle cell apoptosis and aortic remodeling induction in SHR |
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