Consequences of reduced production of NO on vascular reactivity of porcine coronary arteries after angioplasty: importance of EDHF
The consequences of the reduced production of nitric oxide (NO) by cells from regenerated endothelium were investigated by measuring membrane potential of smooth muscle cells (SMCs), isometric tension and cyclic nucleotides content in porcine coronary arteries with intimal thickening, four weeks fol...
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| creator | Thollon, Catherine Fournet‐Bourguignon, Marie Pierre Saboureau, Delphine Lesage, Ludovic Reure, Hélène Vanhoutte, Paul M Vilaine, Jean Paul |
| description | The consequences of the reduced production of nitric oxide (NO) by cells from regenerated endothelium were investigated by measuring membrane potential of smooth muscle cells (SMCs), isometric tension and cyclic nucleotides content in porcine coronary arteries with intimal thickening, four weeks following angioplasty.
Under basal conditions, SMCs of coronary arteries with regenerated endothelium were depolarized by 10 mV. This depolarization was associated with 82% decreased level of cGMP without alteration in cAMP.
Sodium nitroprusside (SNP, 1 μM) repolarized SMCs of the previously denuded coronary arteries. This repolarization was abolished by 1H‐[1,2,4]‐oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ, 10 μM) and not suppressed by glibenclamide (10 μM), iberiotoxin (IbTX, 100 nM) and the combination of charybdotoxin (ChTX, 40 nM) plus apamin (100 nM).
Four‐aminopyridine (4‐AP, 1‐5 mM) generated spontaneous rhythmic activities only in coronary arteries with regenerated endothelium which were abolished by SNP. Nevertheless, 4‐AP did not suppress the repolarization induced by SNP.
In vascular segments with regenerated endothelium, contracted with prostaglandin F2α (PGF2α), relaxation to bradykinin (BK, 30 nM) was unaltered despite a reduced production of cGMP (−70%). Indomethacin (10 μM) plus Nω‐nitro‐L‐arginine (L‐NA, 30 μM) reduced relaxation (−12% and −35% for native and regenerated endothelium, respectively) but did not abolish it.
The hyperpolarizations induced by BK were not altered by the presence of indomethacin and L‐NA and were unchanged in segments with regenerated endothelium.
These data are consistent with a contribution of impairment in NO production to the depolarization of SMCs. Nevertheless, EDHF responses to BK are sufficient to maintain a normal relaxation after angioplasty.
British Journal of Pharmacology (2002) 136, 1153–1161. doi:10.1038/sj.bjp.0704828 |
| doi_str_mv | 10.1038/sj.bjp.0704828 |
| format | Article |
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Under basal conditions, SMCs of coronary arteries with regenerated endothelium were depolarized by 10 mV. This depolarization was associated with 82% decreased level of cGMP without alteration in cAMP.
Sodium nitroprusside (SNP, 1 μM) repolarized SMCs of the previously denuded coronary arteries. This repolarization was abolished by 1H‐[1,2,4]‐oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ, 10 μM) and not suppressed by glibenclamide (10 μM), iberiotoxin (IbTX, 100 nM) and the combination of charybdotoxin (ChTX, 40 nM) plus apamin (100 nM).
Four‐aminopyridine (4‐AP, 1‐5 mM) generated spontaneous rhythmic activities only in coronary arteries with regenerated endothelium which were abolished by SNP. Nevertheless, 4‐AP did not suppress the repolarization induced by SNP.
In vascular segments with regenerated endothelium, contracted with prostaglandin F2α (PGF2α), relaxation to bradykinin (BK, 30 nM) was unaltered despite a reduced production of cGMP (−70%). Indomethacin (10 μM) plus Nω‐nitro‐L‐arginine (L‐NA, 30 μM) reduced relaxation (−12% and −35% for native and regenerated endothelium, respectively) but did not abolish it.
The hyperpolarizations induced by BK were not altered by the presence of indomethacin and L‐NA and were unchanged in segments with regenerated endothelium.
These data are consistent with a contribution of impairment in NO production to the depolarization of SMCs. Nevertheless, EDHF responses to BK are sufficient to maintain a normal relaxation after angioplasty.
British Journal of Pharmacology (2002) 136, 1153–1161. doi:10.1038/sj.bjp.0704828</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0704828</identifier><identifier>PMID: 12163348</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>4-Aminopyridine - pharmacology ; Angioplasty, Balloon, Coronary ; Animals ; Biological and medical sciences ; Biological Factors - pharmacology ; Biological Factors - physiology ; Blood vessels and receptors ; bradykinin ; Bradykinin - pharmacology ; Coronary Vessels - drug effects ; Coronary Vessels - metabolism ; Coronary Vessels - physiology ; Cyclic GMP - biosynthesis ; cyclic nucleotides ; Dinoprost - pharmacology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiology ; endothelium‐derived hyperpolarizing factor ; Fundamental and applied biological sciences. Psychology ; In Vitro Techniques ; Isometric Contraction - drug effects ; Membrane Potentials ; Muscle Relaxation - drug effects ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - physiology ; nitric oxide ; Nitric Oxide - biosynthesis ; Nitric Oxide Donors - pharmacology ; Nitroprusside - pharmacology ; Potassium Channels - drug effects ; Regenerated endothelium ; Regeneration ; Swine ; Vasodilator Agents - pharmacology ; Vertebrates: cardiovascular system</subject><ispartof>British journal of pharmacology, 2002-08, Vol.136 (8), p.1153-1161</ispartof><rights>2002 British Pharmacological Society</rights><rights>2002 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Aug 2002</rights><rights>Copyright 2002, Nature Publishing Group 2002 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4879-d4d0893842b38e3530d157435b28c8deae7c7384b681f8f08cabd600f2b4ea393</citedby><cites>FETCH-LOGICAL-c4879-d4d0893842b38e3530d157435b28c8deae7c7384b681f8f08cabd600f2b4ea393</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/PMC1573455/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573455/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,729,782,786,887,1419,1435,27931,27932,45581,45582,46416,46840,53798,53800</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13849087$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12163348$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Thollon, Catherine</creatorcontrib><creatorcontrib>Fournet‐Bourguignon, Marie Pierre</creatorcontrib><creatorcontrib>Saboureau, Delphine</creatorcontrib><creatorcontrib>Lesage, Ludovic</creatorcontrib><creatorcontrib>Reure, Hélène</creatorcontrib><creatorcontrib>Vanhoutte, Paul M</creatorcontrib><creatorcontrib>Vilaine, Jean Paul</creatorcontrib><title>Consequences of reduced production of NO on vascular reactivity of porcine coronary arteries after angioplasty: importance of EDHF</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>The consequences of the reduced production of nitric oxide (NO) by cells from regenerated endothelium were investigated by measuring membrane potential of smooth muscle cells (SMCs), isometric tension and cyclic nucleotides content in porcine coronary arteries with intimal thickening, four weeks following angioplasty.
Under basal conditions, SMCs of coronary arteries with regenerated endothelium were depolarized by 10 mV. This depolarization was associated with 82% decreased level of cGMP without alteration in cAMP.
Sodium nitroprusside (SNP, 1 μM) repolarized SMCs of the previously denuded coronary arteries. This repolarization was abolished by 1H‐[1,2,4]‐oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ, 10 μM) and not suppressed by glibenclamide (10 μM), iberiotoxin (IbTX, 100 nM) and the combination of charybdotoxin (ChTX, 40 nM) plus apamin (100 nM).
Four‐aminopyridine (4‐AP, 1‐5 mM) generated spontaneous rhythmic activities only in coronary arteries with regenerated endothelium which were abolished by SNP. Nevertheless, 4‐AP did not suppress the repolarization induced by SNP.
In vascular segments with regenerated endothelium, contracted with prostaglandin F2α (PGF2α), relaxation to bradykinin (BK, 30 nM) was unaltered despite a reduced production of cGMP (−70%). Indomethacin (10 μM) plus Nω‐nitro‐L‐arginine (L‐NA, 30 μM) reduced relaxation (−12% and −35% for native and regenerated endothelium, respectively) but did not abolish it.
The hyperpolarizations induced by BK were not altered by the presence of indomethacin and L‐NA and were unchanged in segments with regenerated endothelium.
These data are consistent with a contribution of impairment in NO production to the depolarization of SMCs. Nevertheless, EDHF responses to BK are sufficient to maintain a normal relaxation after angioplasty.
British Journal of Pharmacology (2002) 136, 1153–1161. doi:10.1038/sj.bjp.0704828</description><subject>4-Aminopyridine - pharmacology</subject><subject>Angioplasty, Balloon, Coronary</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biological Factors - pharmacology</subject><subject>Biological Factors - physiology</subject><subject>Blood vessels and receptors</subject><subject>bradykinin</subject><subject>Bradykinin - pharmacology</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - metabolism</subject><subject>Coronary Vessels - physiology</subject><subject>Cyclic GMP - biosynthesis</subject><subject>cyclic nucleotides</subject><subject>Dinoprost - pharmacology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiology</subject><subject>endothelium‐derived hyperpolarizing factor</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>In Vitro Techniques</subject><subject>Isometric Contraction - drug effects</subject><subject>Membrane Potentials</subject><subject>Muscle Relaxation - drug effects</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>nitric oxide</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>Nitroprusside - pharmacology</subject><subject>Potassium Channels - drug effects</subject><subject>Regenerated endothelium</subject><subject>Regeneration</subject><subject>Swine</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc1v1DAQxS1ERbeFK0cUIbW3LP5K7HBAKkvbRaooBzhbjuMUR1k72MmivfKXM9FGFLhw8sjv5zfjeQi9JHhNMJNvUreuu2GNBeaSyidoRbgo84JJ8hStMMYiJ0TKU3SWUocxiKJ4hk4JJSVjXK7Qz03wyX6frDc2ZaHNom0mY5tsiAGK0QU_3366z6DY62SmXkeANEh7Nx5mcQjROG8zE2LwOh4yHUcbHfjpFopM-wcXhl6n8fA2czvARw3t5qfXH7Y3z9FJq_tkXyznOfp6c_1ls83v7m8_bq7ucsOlqPKGN1hWTHJaM2lZwXBDCsFZUVNpZGO1FUaAXJeStLLF0ui6KTFuac2tZhU7R--OvsNU72xjrB-j7tUQ3Q6GVkE79bfi3Tf1EPYK2jBeFGBwuRjEABtLo9q5ZGzfa2_DlJQglSgppwC-_gfswhQ9fE5RIogUlMzQ-giZGFKKtv09CcFqzlalTkG2askWHrz6c_5HfAkTgIsFgJx030bYskuPHCynwlIAx47cD9fbw3_aqveft1xUFfsFICDAWw</recordid><startdate>200208</startdate><enddate>200208</enddate><creator>Thollon, Catherine</creator><creator>Fournet‐Bourguignon, Marie Pierre</creator><creator>Saboureau, Delphine</creator><creator>Lesage, Ludovic</creator><creator>Reure, Hélène</creator><creator>Vanhoutte, Paul M</creator><creator>Vilaine, Jean Paul</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>200208</creationdate><title>Consequences of reduced production of NO on vascular reactivity of porcine coronary arteries after angioplasty: importance of EDHF</title><author>Thollon, Catherine ; Fournet‐Bourguignon, Marie Pierre ; Saboureau, Delphine ; Lesage, Ludovic ; Reure, Hélène ; Vanhoutte, Paul M ; Vilaine, Jean Paul</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4879-d4d0893842b38e3530d157435b28c8deae7c7384b681f8f08cabd600f2b4ea393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>4-Aminopyridine - pharmacology</topic><topic>Angioplasty, Balloon, Coronary</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biological Factors - pharmacology</topic><topic>Biological Factors - physiology</topic><topic>Blood vessels and receptors</topic><topic>bradykinin</topic><topic>Bradykinin - pharmacology</topic><topic>Coronary Vessels - drug effects</topic><topic>Coronary Vessels - metabolism</topic><topic>Coronary Vessels - physiology</topic><topic>Cyclic GMP - biosynthesis</topic><topic>cyclic nucleotides</topic><topic>Dinoprost - pharmacology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - physiology</topic><topic>endothelium‐derived hyperpolarizing factor</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>In Vitro Techniques</topic><topic>Isometric Contraction - drug effects</topic><topic>Membrane Potentials</topic><topic>Muscle Relaxation - drug effects</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>nitric oxide</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Nitroprusside - pharmacology</topic><topic>Potassium Channels - drug effects</topic><topic>Regenerated endothelium</topic><topic>Regeneration</topic><topic>Swine</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Thollon, Catherine</creatorcontrib><creatorcontrib>Fournet‐Bourguignon, Marie Pierre</creatorcontrib><creatorcontrib>Saboureau, Delphine</creatorcontrib><creatorcontrib>Lesage, Ludovic</creatorcontrib><creatorcontrib>Reure, Hélène</creatorcontrib><creatorcontrib>Vanhoutte, Paul M</creatorcontrib><creatorcontrib>Vilaine, Jean Paul</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>MEDLINE - Academic</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>Thollon, Catherine</au><au>Fournet‐Bourguignon, Marie Pierre</au><au>Saboureau, Delphine</au><au>Lesage, Ludovic</au><au>Reure, Hélène</au><au>Vanhoutte, Paul M</au><au>Vilaine, Jean Paul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Consequences of reduced production of NO on vascular reactivity of porcine coronary arteries after angioplasty: importance of EDHF</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2002-08</date><risdate>2002</risdate><volume>136</volume><issue>8</issue><spage>1153</spage><epage>1161</epage><pages>1153-1161</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>The consequences of the reduced production of nitric oxide (NO) by cells from regenerated endothelium were investigated by measuring membrane potential of smooth muscle cells (SMCs), isometric tension and cyclic nucleotides content in porcine coronary arteries with intimal thickening, four weeks following angioplasty.
Under basal conditions, SMCs of coronary arteries with regenerated endothelium were depolarized by 10 mV. This depolarization was associated with 82% decreased level of cGMP without alteration in cAMP.
Sodium nitroprusside (SNP, 1 μM) repolarized SMCs of the previously denuded coronary arteries. This repolarization was abolished by 1H‐[1,2,4]‐oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ, 10 μM) and not suppressed by glibenclamide (10 μM), iberiotoxin (IbTX, 100 nM) and the combination of charybdotoxin (ChTX, 40 nM) plus apamin (100 nM).
Four‐aminopyridine (4‐AP, 1‐5 mM) generated spontaneous rhythmic activities only in coronary arteries with regenerated endothelium which were abolished by SNP. Nevertheless, 4‐AP did not suppress the repolarization induced by SNP.
In vascular segments with regenerated endothelium, contracted with prostaglandin F2α (PGF2α), relaxation to bradykinin (BK, 30 nM) was unaltered despite a reduced production of cGMP (−70%). Indomethacin (10 μM) plus Nω‐nitro‐L‐arginine (L‐NA, 30 μM) reduced relaxation (−12% and −35% for native and regenerated endothelium, respectively) but did not abolish it.
The hyperpolarizations induced by BK were not altered by the presence of indomethacin and L‐NA and were unchanged in segments with regenerated endothelium.
These data are consistent with a contribution of impairment in NO production to the depolarization of SMCs. Nevertheless, EDHF responses to BK are sufficient to maintain a normal relaxation after angioplasty.
British Journal of Pharmacology (2002) 136, 1153–1161. doi:10.1038/sj.bjp.0704828</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>12163348</pmid><doi>10.1038/sj.bjp.0704828</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 4-Aminopyridine - pharmacology Angioplasty, Balloon, Coronary Animals Biological and medical sciences Biological Factors - pharmacology Biological Factors - physiology Blood vessels and receptors bradykinin Bradykinin - pharmacology Coronary Vessels - drug effects Coronary Vessels - metabolism Coronary Vessels - physiology Cyclic GMP - biosynthesis cyclic nucleotides Dinoprost - pharmacology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Endothelium, Vascular - physiology endothelium‐derived hyperpolarizing factor Fundamental and applied biological sciences. Psychology In Vitro Techniques Isometric Contraction - drug effects Membrane Potentials Muscle Relaxation - drug effects Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - physiology nitric oxide Nitric Oxide - biosynthesis Nitric Oxide Donors - pharmacology Nitroprusside - pharmacology Potassium Channels - drug effects Regenerated endothelium Regeneration Swine Vasodilator Agents - pharmacology Vertebrates: cardiovascular system |
| title | Consequences of reduced production of NO on vascular reactivity of porcine coronary arteries after angioplasty: importance of EDHF |
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