Telmisartan Decreases Plasma Levels of Asymmetrical Dimethyl-L-Arginine and Improves Lipid and Glucose Metabolism and Vascular Function
Telmisartan is an angiotensin II receptor blocker (ARB) and also an activator of peroxisome proliferator-activated receptor-γ (PPAR-γ). We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide s...
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| Veröffentlicht in: | International Heart Journal 2009, Vol.50(1), pp.73-83 |
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| creator | Ono, Yoshifumi Nakaya, Yutaka Bando, Shigenobu Soeki, Takeshi Ito, Susumu Sata, Masataka |
| description | Telmisartan is an angiotensin II receptor blocker (ARB) and also an activator of peroxisome proliferator-activated receptor-γ (PPAR-γ). We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-γ. Telmisartan was administered to 15 patients with essential hypertension. To assess vascular function, asymmetric dimethylarginine (ADMA), an eNOS inhibitor synthesized by endothelial cells, and the pulse-wave velocity (PWV) were measured. The serum levels of lipid, glucose, and glycohemoglobin (HbA1c) were also evaluated before and after treatment. Telmisartan therapy significantly decreased the blood pressure and total- and LDL-cholesterol levels. HbA1c was also significantly improved but not in fasting plasma glucose. The serum levels of ADMA were significantly decreased (0.48 ± 0.08 to 0.42 ± 0.05 nmol/mL; P = 0.01). PWV values were significantly decreased by telmisartan from 1,822.5 ± 352.3 to 1,661.5 ± 299.8 cm/second (P = 0.04*). Telmisartan decreased PWV presumably via the activation of PPAR-γ, suggesting that this agent improves vascular endothelial function via its pleiotropic effects, a mechanism that is different from its hypotensive effects. |
| doi_str_mv | 10.1536/ihj.50.73 |
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We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-γ. Telmisartan was administered to 15 patients with essential hypertension. To assess vascular function, asymmetric dimethylarginine (ADMA), an eNOS inhibitor synthesized by endothelial cells, and the pulse-wave velocity (PWV) were measured. The serum levels of lipid, glucose, and glycohemoglobin (HbA1c) were also evaluated before and after treatment. Telmisartan therapy significantly decreased the blood pressure and total- and LDL-cholesterol levels. HbA1c was also significantly improved but not in fasting plasma glucose. The serum levels of ADMA were significantly decreased (0.48 ± 0.08 to 0.42 ± 0.05 nmol/mL; P = 0.01). PWV values were significantly decreased by telmisartan from 1,822.5 ± 352.3 to 1,661.5 ± 299.8 cm/second (P = 0.04*). Telmisartan decreased PWV presumably via the activation of PPAR-γ, suggesting that this agent improves vascular endothelial function via its pleiotropic effects, a mechanism that is different from its hypotensive effects.</description><identifier>ISSN: 1349-2365</identifier><identifier>EISSN: 1349-3299</identifier><identifier>DOI: 10.1536/ihj.50.73</identifier><identifier>PMID: 19246848</identifier><language>eng</language><publisher>Japan: International Heart Journal Association</publisher><subject><![CDATA[ADMA ; Administration, Oral ; Aged ; Angiotensin II Type 1 Receptor Blockers - administration & dosage ; Angiotensin II Type 1 Receptor Blockers - therapeutic use ; Arginine - analogs & derivatives ; Arginine - antagonists & inhibitors ; Arginine - blood ; Benzimidazoles - administration & dosage ; Benzimidazoles - therapeutic use ; Benzoates - administration & dosage ; Benzoates - therapeutic use ; Blood Glucose - drug effects ; Blood Glucose - metabolism ; Blood Pressure - drug effects ; Cholesterol, LDL - blood ; Cholesterol, LDL - drug effects ; Dose-Response Relationship, Drug ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiopathology ; Essential hypertension ; Female ; Humans ; Hypertension - blood ; Hypertension - drug therapy ; Hypertension - physiopathology ; Male ; Nitric Oxide Synthase Type III - antagonists & inhibitors ; Nitric Oxide Synthase Type III - biosynthesis ; PPAR gamma - drug effects ; PPAR gamma - metabolism ; PPAR-γ ; Telmisartan ; Treatment Outcome ; Vascular endothelial function]]></subject><ispartof>International Heart Journal, 2009, Vol.50(1), pp.73-83</ispartof><rights>2009 by the International Heart Journal Association</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-cf2fd389b6260182a5d422d1fbdf02e6de091879a4388239bcc2fab00a57c7d93</citedby><cites>FETCH-LOGICAL-c496t-cf2fd389b6260182a5d422d1fbdf02e6de091879a4388239bcc2fab00a57c7d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19246848$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ono, Yoshifumi</creatorcontrib><creatorcontrib>Nakaya, Yutaka</creatorcontrib><creatorcontrib>Bando, Shigenobu</creatorcontrib><creatorcontrib>Soeki, Takeshi</creatorcontrib><creatorcontrib>Ito, Susumu</creatorcontrib><creatorcontrib>Sata, Masataka</creatorcontrib><title>Telmisartan Decreases Plasma Levels of Asymmetrical Dimethyl-L-Arginine and Improves Lipid and Glucose Metabolism and Vascular Function</title><title>International Heart Journal</title><addtitle>Int. Heart J.</addtitle><description>Telmisartan is an angiotensin II receptor blocker (ARB) and also an activator of peroxisome proliferator-activated receptor-γ (PPAR-γ). We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-γ. Telmisartan was administered to 15 patients with essential hypertension. To assess vascular function, asymmetric dimethylarginine (ADMA), an eNOS inhibitor synthesized by endothelial cells, and the pulse-wave velocity (PWV) were measured. The serum levels of lipid, glucose, and glycohemoglobin (HbA1c) were also evaluated before and after treatment. Telmisartan therapy significantly decreased the blood pressure and total- and LDL-cholesterol levels. HbA1c was also significantly improved but not in fasting plasma glucose. The serum levels of ADMA were significantly decreased (0.48 ± 0.08 to 0.42 ± 0.05 nmol/mL; P = 0.01). PWV values were significantly decreased by telmisartan from 1,822.5 ± 352.3 to 1,661.5 ± 299.8 cm/second (P = 0.04*). Telmisartan decreased PWV presumably via the activation of PPAR-γ, suggesting that this agent improves vascular endothelial function via its pleiotropic effects, a mechanism that is different from its hypotensive effects.</description><subject>ADMA</subject><subject>Administration, Oral</subject><subject>Aged</subject><subject>Angiotensin II Type 1 Receptor Blockers - administration & dosage</subject><subject>Angiotensin II Type 1 Receptor Blockers - therapeutic use</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - antagonists & inhibitors</subject><subject>Arginine - blood</subject><subject>Benzimidazoles - administration & dosage</subject><subject>Benzimidazoles - therapeutic use</subject><subject>Benzoates - administration & dosage</subject><subject>Benzoates - therapeutic use</subject><subject>Blood Glucose - drug effects</subject><subject>Blood Glucose - metabolism</subject><subject>Blood Pressure - drug effects</subject><subject>Cholesterol, LDL - blood</subject><subject>Cholesterol, LDL - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Essential hypertension</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension - blood</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - physiopathology</subject><subject>Male</subject><subject>Nitric Oxide Synthase Type III - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase Type III - biosynthesis</subject><subject>PPAR gamma - drug effects</subject><subject>PPAR gamma - metabolism</subject><subject>PPAR-γ</subject><subject>Telmisartan</subject><subject>Treatment Outcome</subject><subject>Vascular endothelial function</subject><issn>1349-2365</issn><issn>1349-3299</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1v1DAQhi0Eoh9w4A8gn5A4ZOuPxIkvSKuWlkpBcChcrYk96XrlJIudVNpfwN-u6S7tZWY088yrmZeQD5yteCXVhd9sVxVb1fIVOeWy1IUUWr8-1kKq6oScpbRlrOQVq9-SE65FqZqyOSV_7zAMPkGcYaRXaCNCwkR_BkgD0BYfMCQ69XSd9sOAc_QWAr3yudzsQ9EW63jvRz8ihdHR22EXp4e83vqdd0-tm7DYKSH9jjN0U_BpeGr_hmSXAJFeL6Od_TS-I296CAnfH_M5-XX99e7yW9H-uLm9XLeFLbWaC9uL3slGd0ooxhsBlSuFcLzvXM8EKodM86bWUMqmEVJ31ooeOsagqm3ttDwnnw66-dI_C6bZ5O8thgAjTksySulaqLLO4OcDaOOUUsTe7KIfIO4NZ-af6ya7bipmapnZj0fRpRvQvZBHmzPw5QBs0wz3-Axk270N-F-KH0Itnwd2A9HgKB8BjWOWUQ</recordid><startdate>2009</startdate><enddate>2009</enddate><creator>Ono, Yoshifumi</creator><creator>Nakaya, Yutaka</creator><creator>Bando, Shigenobu</creator><creator>Soeki, Takeshi</creator><creator>Ito, Susumu</creator><creator>Sata, Masataka</creator><general>International Heart Journal Association</general><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>7X8</scope></search><sort><creationdate>2009</creationdate><title>Telmisartan Decreases Plasma Levels of Asymmetrical Dimethyl-L-Arginine and Improves Lipid and Glucose Metabolism and Vascular Function</title><author>Ono, Yoshifumi ; Nakaya, Yutaka ; Bando, Shigenobu ; Soeki, Takeshi ; Ito, Susumu ; Sata, Masataka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-cf2fd389b6260182a5d422d1fbdf02e6de091879a4388239bcc2fab00a57c7d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>ADMA</topic><topic>Administration, Oral</topic><topic>Aged</topic><topic>Angiotensin II Type 1 Receptor Blockers - administration & dosage</topic><topic>Angiotensin II Type 1 Receptor Blockers - therapeutic use</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - antagonists & inhibitors</topic><topic>Arginine - blood</topic><topic>Benzimidazoles - administration & dosage</topic><topic>Benzimidazoles - therapeutic use</topic><topic>Benzoates - administration & dosage</topic><topic>Benzoates - therapeutic use</topic><topic>Blood Glucose - drug effects</topic><topic>Blood Glucose - metabolism</topic><topic>Blood Pressure - drug effects</topic><topic>Cholesterol, LDL - blood</topic><topic>Cholesterol, LDL - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Essential hypertension</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension - blood</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - physiopathology</topic><topic>Male</topic><topic>Nitric Oxide Synthase Type III - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase Type III - biosynthesis</topic><topic>PPAR gamma - drug effects</topic><topic>PPAR gamma - metabolism</topic><topic>PPAR-γ</topic><topic>Telmisartan</topic><topic>Treatment Outcome</topic><topic>Vascular endothelial function</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ono, Yoshifumi</creatorcontrib><creatorcontrib>Nakaya, Yutaka</creatorcontrib><creatorcontrib>Bando, Shigenobu</creatorcontrib><creatorcontrib>Soeki, Takeshi</creatorcontrib><creatorcontrib>Ito, Susumu</creatorcontrib><creatorcontrib>Sata, Masataka</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>International Heart Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ono, Yoshifumi</au><au>Nakaya, Yutaka</au><au>Bando, Shigenobu</au><au>Soeki, Takeshi</au><au>Ito, Susumu</au><au>Sata, Masataka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Telmisartan Decreases Plasma Levels of Asymmetrical Dimethyl-L-Arginine and Improves Lipid and Glucose Metabolism and Vascular Function</atitle><jtitle>International Heart Journal</jtitle><addtitle>Int. Heart J.</addtitle><date>2009</date><risdate>2009</risdate><volume>50</volume><issue>1</issue><spage>73</spage><epage>83</epage><pages>73-83</pages><issn>1349-2365</issn><eissn>1349-3299</eissn><abstract>Telmisartan is an angiotensin II receptor blocker (ARB) and also an activator of peroxisome proliferator-activated receptor-γ (PPAR-γ). We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-γ. Telmisartan was administered to 15 patients with essential hypertension. To assess vascular function, asymmetric dimethylarginine (ADMA), an eNOS inhibitor synthesized by endothelial cells, and the pulse-wave velocity (PWV) were measured. The serum levels of lipid, glucose, and glycohemoglobin (HbA1c) were also evaluated before and after treatment. Telmisartan therapy significantly decreased the blood pressure and total- and LDL-cholesterol levels. HbA1c was also significantly improved but not in fasting plasma glucose. The serum levels of ADMA were significantly decreased (0.48 ± 0.08 to 0.42 ± 0.05 nmol/mL; P = 0.01). PWV values were significantly decreased by telmisartan from 1,822.5 ± 352.3 to 1,661.5 ± 299.8 cm/second (P = 0.04*). Telmisartan decreased PWV presumably via the activation of PPAR-γ, suggesting that this agent improves vascular endothelial function via its pleiotropic effects, a mechanism that is different from its hypotensive effects.</abstract><cop>Japan</cop><pub>International Heart Journal Association</pub><pmid>19246848</pmid><doi>10.1536/ihj.50.73</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International Heart Journal, 2009, Vol.50(1), pp.73-83 |
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| subjects | ADMA Administration, Oral Aged Angiotensin II Type 1 Receptor Blockers - administration & dosage Angiotensin II Type 1 Receptor Blockers - therapeutic use Arginine - analogs & derivatives Arginine - antagonists & inhibitors Arginine - blood Benzimidazoles - administration & dosage Benzimidazoles - therapeutic use Benzoates - administration & dosage Benzoates - therapeutic use Blood Glucose - drug effects Blood Glucose - metabolism Blood Pressure - drug effects Cholesterol, LDL - blood Cholesterol, LDL - drug effects Dose-Response Relationship, Drug Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Endothelium, Vascular - physiopathology Essential hypertension Female Humans Hypertension - blood Hypertension - drug therapy Hypertension - physiopathology Male Nitric Oxide Synthase Type III - antagonists & inhibitors Nitric Oxide Synthase Type III - biosynthesis PPAR gamma - drug effects PPAR gamma - metabolism PPAR-γ Telmisartan Treatment Outcome Vascular endothelial function |
| title | Telmisartan Decreases Plasma Levels of Asymmetrical Dimethyl-L-Arginine and Improves Lipid and Glucose Metabolism and Vascular Function |
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