PDE5 Inhibitor Sildenafil Citrate Augments Endothelium-Dependent Vasodilation in Smokers
ABSTRACT—Smoking is associated with endothelial dysfunction. The purpose of this study was to determine the effect of sildenafil, an inhibitor of phosphodiesterase type 5 (PDE5), on endothelial function in smokers. We evaluated the forearm blood flow (FBF) responses to acetylcholine (ACh), an endoth...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2003-05, Vol.41 (5), p.1106-1110 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Kimura, Masashi Higashi, Yukihito Hara, Keiko Noma, Kensuke Sasaki, Satoshi Nakagawa, Keigo Goto, Chikara Oshima, Tetsuya Yoshizumi, Masao Chayama, Kazuaki |
| description | ABSTRACT—Smoking is associated with endothelial dysfunction. The purpose of this study was to determine the effect of sildenafil, an inhibitor of phosphodiesterase type 5 (PDE5), on endothelial function in smokers. We evaluated the forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, before and after oral sildenafil administration (100 mg) with a strain-gauge plethysmograph in 10 young healthy male smokers and 10 young healthy male nonsmokers. FBF response to ACh was lower in smokers than in nonsmokers. The vasodilatory effects of SNP were similar in both groups. Sildenafil increased the FBF response to ACh from 9.3±2.0 to 12.5±3.5 mL/min per 100 mL tissue in smokers and from 12.6±5.6 to 19.6±8.4 mL/min per 100 mL tissue in nonsmokers, and it increased the response to SNP from 13.3±3.9 to 15.1±4.3 mL/min per 100 mL tissue in smokers and from 14.8±5.2 to 18.4±6.0 mL/min/100 mL tissue in nonsmokers (P |
| doi_str_mv | 10.1161/01.HYP.0000068202.42431.CC |
| format | Article |
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The purpose of this study was to determine the effect of sildenafil, an inhibitor of phosphodiesterase type 5 (PDE5), on endothelial function in smokers. We evaluated the forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, before and after oral sildenafil administration (100 mg) with a strain-gauge plethysmograph in 10 young healthy male smokers and 10 young healthy male nonsmokers. FBF response to ACh was lower in smokers than in nonsmokers. The vasodilatory effects of SNP were similar in both groups. Sildenafil increased the FBF response to ACh from 9.3±2.0 to 12.5±3.5 mL/min per 100 mL tissue in smokers and from 12.6±5.6 to 19.6±8.4 mL/min per 100 mL tissue in nonsmokers, and it increased the response to SNP from 13.3±3.9 to 15.1±4.3 mL/min per 100 mL tissue in smokers and from 14.8±5.2 to 18.4±6.0 mL/min/100 mL tissue in nonsmokers (P <0.05 for all). The ratio of maximal ACh-stimulated FBF expressed as a ratio of maximal SNP-stimulated FBF significantly increased after administration of sildenafil in both groups. Infusion of N-monomethyl-l-arginine, a nitric oxide synthase inhibitor, abolished sildenafil-induced augmentation of the FBF response to ACh in both groups. The findings suggest that endothelial function is impaired in smokers compared with that in nonsmokers, that inhibition of PDE5 by sildenafil significantly increases nitric oxide-mediated vasodilation, and that the activities of PDE5 in smokers and nonsmokers may be similar.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000068202.42431.CC</identifier><identifier>PMID: 12695418</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>3',5'-Cyclic-GMP Phosphodiesterases - antagonists & inhibitors ; Acetylcholine - pharmacology ; Administration, Oral ; Adult ; Biological and medical sciences ; Blood Pressure - drug effects ; Body Mass Index ; Cardiovascular system ; Cyclic Nucleotide Phosphodiesterases, Type 5 ; Dose-Response Relationship, Drug ; Endothelium - physiology ; Enzyme Inhibitors - pharmacology ; Forearm - blood supply ; Heart Rate - drug effects ; Humans ; Infant ; Male ; Medical sciences ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitroprusside - pharmacology ; omega-N-Methylarginine - pharmacology ; Pharmacology. Drug treatments ; Phosphodiesterase Inhibitors - administration & dosage ; Phosphodiesterase Inhibitors - pharmacology ; Piperazines - administration & dosage ; Piperazines - pharmacology ; Purines ; Regional Blood Flow - drug effects ; Sildenafil Citrate ; Smoking ; Sulfones ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology ; Vasodilator agents. Cerebral vasodilators</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2003-05, Vol.41 (5), p.1106-1110</ispartof><rights>2003 American Heart Association, Inc.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. May 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5770-97ed080ee44971559a6476a2b0e65a78641be12eba4283777ce2244914dcaf9c3</citedby><cites>FETCH-LOGICAL-c5770-97ed080ee44971559a6476a2b0e65a78641be12eba4283777ce2244914dcaf9c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3673,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14785808$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12695418$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kimura, Masashi</creatorcontrib><creatorcontrib>Higashi, Yukihito</creatorcontrib><creatorcontrib>Hara, Keiko</creatorcontrib><creatorcontrib>Noma, Kensuke</creatorcontrib><creatorcontrib>Sasaki, Satoshi</creatorcontrib><creatorcontrib>Nakagawa, Keigo</creatorcontrib><creatorcontrib>Goto, Chikara</creatorcontrib><creatorcontrib>Oshima, Tetsuya</creatorcontrib><creatorcontrib>Yoshizumi, Masao</creatorcontrib><creatorcontrib>Chayama, Kazuaki</creatorcontrib><title>PDE5 Inhibitor Sildenafil Citrate Augments Endothelium-Dependent Vasodilation in Smokers</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>ABSTRACT—Smoking is associated with endothelial dysfunction. The purpose of this study was to determine the effect of sildenafil, an inhibitor of phosphodiesterase type 5 (PDE5), on endothelial function in smokers. We evaluated the forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, before and after oral sildenafil administration (100 mg) with a strain-gauge plethysmograph in 10 young healthy male smokers and 10 young healthy male nonsmokers. FBF response to ACh was lower in smokers than in nonsmokers. The vasodilatory effects of SNP were similar in both groups. Sildenafil increased the FBF response to ACh from 9.3±2.0 to 12.5±3.5 mL/min per 100 mL tissue in smokers and from 12.6±5.6 to 19.6±8.4 mL/min per 100 mL tissue in nonsmokers, and it increased the response to SNP from 13.3±3.9 to 15.1±4.3 mL/min per 100 mL tissue in smokers and from 14.8±5.2 to 18.4±6.0 mL/min/100 mL tissue in nonsmokers (P <0.05 for all). The ratio of maximal ACh-stimulated FBF expressed as a ratio of maximal SNP-stimulated FBF significantly increased after administration of sildenafil in both groups. Infusion of N-monomethyl-l-arginine, a nitric oxide synthase inhibitor, abolished sildenafil-induced augmentation of the FBF response to ACh in both groups. The findings suggest that endothelial function is impaired in smokers compared with that in nonsmokers, that inhibition of PDE5 by sildenafil significantly increases nitric oxide-mediated vasodilation, and that the activities of PDE5 in smokers and nonsmokers may be similar.</description><subject>3',5'-Cyclic-GMP Phosphodiesterases - antagonists & inhibitors</subject><subject>Acetylcholine - pharmacology</subject><subject>Administration, Oral</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Body Mass Index</subject><subject>Cardiovascular system</subject><subject>Cyclic Nucleotide Phosphodiesterases, Type 5</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelium - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Forearm - blood supply</subject><subject>Heart Rate - drug effects</subject><subject>Humans</subject><subject>Infant</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitroprusside - pharmacology</subject><subject>omega-N-Methylarginine - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphodiesterase Inhibitors - administration & dosage</subject><subject>Phosphodiesterase Inhibitors - pharmacology</subject><subject>Piperazines - administration & dosage</subject><subject>Piperazines - pharmacology</subject><subject>Purines</subject><subject>Regional Blood Flow - drug effects</subject><subject>Sildenafil Citrate</subject><subject>Smoking</subject><subject>Sulfones</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vasodilator agents. Cerebral vasodilators</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkGFr3CAYx2VsrNduX2GEwvYumRqNZu9KelsLhRW6je6VmOTJztboTQ1l375e7-BgD8iD8Pv7lx9C5wRXhDTkMybV1e_bCu-mkRTTilFWk6rrXqEV4ZSVjDf1a7TCpGVlS8j9CTqN8QFjwhgTb9EJoU3LGZErdH97uebFtduY3iQfijtjR3B6MrboTAo6QXGx_JnBpVis3ejTBqxZ5vIStuAymYpfOvrRWJ2Md4Vxxd3sHyHEd-jNpG2E94d9hn5-Xf_orsqb79-uu4ubcuBC4LIVMGKJARhrBeG81Q0TjaY9hoZrIRtGeiAUes2orIUQA1CaWcLGQU_tUJ-hT_t3t8H_XSAmNZs4gLXagV-iEjXNScYzeP4f-OCX4PLfFMWcyp24DH3ZQ0PwMQaY1DaYWYd_imC1k68wUVm-OspXL_JV1-Xwh0PD0s8wHqMH2xn4eAB0HLSdgnaDiUeOCckl3nFszz15m7LLR7s8QVAb0DZtXqoZbWRJMa4xz7cyH4rrZ4zwm7E</recordid><startdate>200305</startdate><enddate>200305</enddate><creator>Kimura, Masashi</creator><creator>Higashi, Yukihito</creator><creator>Hara, Keiko</creator><creator>Noma, Kensuke</creator><creator>Sasaki, Satoshi</creator><creator>Nakagawa, Keigo</creator><creator>Goto, Chikara</creator><creator>Oshima, Tetsuya</creator><creator>Yoshizumi, Masao</creator><creator>Chayama, Kazuaki</creator><general>American Heart Association, Inc</general><general>Lippincott</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>K9.</scope><scope>7X8</scope></search><sort><creationdate>200305</creationdate><title>PDE5 Inhibitor Sildenafil Citrate Augments Endothelium-Dependent Vasodilation in Smokers</title><author>Kimura, Masashi ; Higashi, Yukihito ; Hara, Keiko ; Noma, Kensuke ; Sasaki, Satoshi ; Nakagawa, Keigo ; Goto, Chikara ; Oshima, Tetsuya ; Yoshizumi, Masao ; Chayama, Kazuaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5770-97ed080ee44971559a6476a2b0e65a78641be12eba4283777ce2244914dcaf9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>3',5'-Cyclic-GMP Phosphodiesterases - antagonists & inhibitors</topic><topic>Acetylcholine - pharmacology</topic><topic>Administration, Oral</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Body Mass Index</topic><topic>Cardiovascular system</topic><topic>Cyclic Nucleotide Phosphodiesterases, Type 5</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelium - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Forearm - blood supply</topic><topic>Heart Rate - drug effects</topic><topic>Humans</topic><topic>Infant</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitroprusside - pharmacology</topic><topic>omega-N-Methylarginine - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphodiesterase Inhibitors - administration & dosage</topic><topic>Phosphodiesterase Inhibitors - pharmacology</topic><topic>Piperazines - administration & dosage</topic><topic>Piperazines - pharmacology</topic><topic>Purines</topic><topic>Regional Blood Flow - drug effects</topic><topic>Sildenafil Citrate</topic><topic>Smoking</topic><topic>Sulfones</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vasodilator agents. Cerebral vasodilators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kimura, Masashi</creatorcontrib><creatorcontrib>Higashi, Yukihito</creatorcontrib><creatorcontrib>Hara, Keiko</creatorcontrib><creatorcontrib>Noma, Kensuke</creatorcontrib><creatorcontrib>Sasaki, Satoshi</creatorcontrib><creatorcontrib>Nakagawa, Keigo</creatorcontrib><creatorcontrib>Goto, Chikara</creatorcontrib><creatorcontrib>Oshima, Tetsuya</creatorcontrib><creatorcontrib>Yoshizumi, Masao</creatorcontrib><creatorcontrib>Chayama, Kazuaki</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 Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kimura, Masashi</au><au>Higashi, Yukihito</au><au>Hara, Keiko</au><au>Noma, Kensuke</au><au>Sasaki, Satoshi</au><au>Nakagawa, Keigo</au><au>Goto, Chikara</au><au>Oshima, Tetsuya</au><au>Yoshizumi, Masao</au><au>Chayama, Kazuaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PDE5 Inhibitor Sildenafil Citrate Augments Endothelium-Dependent Vasodilation in Smokers</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2003-05</date><risdate>2003</risdate><volume>41</volume><issue>5</issue><spage>1106</spage><epage>1110</epage><pages>1106-1110</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>ABSTRACT—Smoking is associated with endothelial dysfunction. The purpose of this study was to determine the effect of sildenafil, an inhibitor of phosphodiesterase type 5 (PDE5), on endothelial function in smokers. We evaluated the forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, before and after oral sildenafil administration (100 mg) with a strain-gauge plethysmograph in 10 young healthy male smokers and 10 young healthy male nonsmokers. FBF response to ACh was lower in smokers than in nonsmokers. The vasodilatory effects of SNP were similar in both groups. Sildenafil increased the FBF response to ACh from 9.3±2.0 to 12.5±3.5 mL/min per 100 mL tissue in smokers and from 12.6±5.6 to 19.6±8.4 mL/min per 100 mL tissue in nonsmokers, and it increased the response to SNP from 13.3±3.9 to 15.1±4.3 mL/min per 100 mL tissue in smokers and from 14.8±5.2 to 18.4±6.0 mL/min/100 mL tissue in nonsmokers (P <0.05 for all). The ratio of maximal ACh-stimulated FBF expressed as a ratio of maximal SNP-stimulated FBF significantly increased after administration of sildenafil in both groups. Infusion of N-monomethyl-l-arginine, a nitric oxide synthase inhibitor, abolished sildenafil-induced augmentation of the FBF response to ACh in both groups. The findings suggest that endothelial function is impaired in smokers compared with that in nonsmokers, that inhibition of PDE5 by sildenafil significantly increases nitric oxide-mediated vasodilation, and that the activities of PDE5 in smokers and nonsmokers may be similar.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>12695418</pmid><doi>10.1161/01.HYP.0000068202.42431.CC</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2003-05, Vol.41 (5), p.1106-1110 |
| issn | 0194-911X 1524-4563 |
| language | eng |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | 3',5'-Cyclic-GMP Phosphodiesterases - antagonists & inhibitors Acetylcholine - pharmacology Administration, Oral Adult Biological and medical sciences Blood Pressure - drug effects Body Mass Index Cardiovascular system Cyclic Nucleotide Phosphodiesterases, Type 5 Dose-Response Relationship, Drug Endothelium - physiology Enzyme Inhibitors - pharmacology Forearm - blood supply Heart Rate - drug effects Humans Infant Male Medical sciences Nitric Oxide Synthase - antagonists & inhibitors Nitroprusside - pharmacology omega-N-Methylarginine - pharmacology Pharmacology. Drug treatments Phosphodiesterase Inhibitors - administration & dosage Phosphodiesterase Inhibitors - pharmacology Piperazines - administration & dosage Piperazines - pharmacology Purines Regional Blood Flow - drug effects Sildenafil Citrate Smoking Sulfones Vasodilation - drug effects Vasodilator Agents - pharmacology Vasodilator agents. Cerebral vasodilators |
| title | PDE5 Inhibitor Sildenafil Citrate Augments Endothelium-Dependent Vasodilation in Smokers |
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