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Changes in prostacyclin, thromboxane A2 and F2-isoprostanes, and influence of eicosapentaenoic acid and antiplatelet agents in patients with hypertension and hyperlipidemia
Prostacyclin (PGI2), thromboxane A2 (TXA2) and F2-isoprostanes, prostaglandin F2-like compounds, have wide and contrasting spectrum of biological activities and may influence blood pressure and atherogenesis. To investigate the dynamics of PGI2, TXA2 and F2-isoprostanes in patients with hypertension...
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Published in: | Immunopharmacology 1999-10, Vol.44 (1-2), p.193-198 |
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creator | Yamada, Masaaki Omata, Ken Abe, Fumiaki Ito, Sadayoshi Keishi Abe |
description | Prostacyclin (PGI2), thromboxane A2 (TXA2) and F2-isoprostanes, prostaglandin F2-like compounds, have wide and contrasting spectrum of biological activities and may influence blood pressure and atherogenesis. To investigate the dynamics of PGI2, TXA2 and F2-isoprostanes in patients with hypertension and hyperlipidemia (HH group), we measured the major urinary metabolites of PGI2: 6-keto PGF1α (Keto) and 2,3-dinor-6-keto PGF1α (Dinor), those of TXA2: TXB2 and 11-dehydro TXB2 (Dehydro), and urinary 8-isoprostane (Iso) in 34 patients. Urinary excretion of Dinor was significantly lower in patients than in controls and that of Dehydro was significantly higher in patients than in controls. Keto, TXB2 and Iso were not significantly different between them. Antiplatelet agents decreased not only TXA2 metabolites but also PGI2 metabolites. Urinary C-peptide immunoreactivity was correlated with Dinor and Dehydro. After administration of eicosapentaenoic acid (EPA), total cholesterol (T-cho) and triglycerides (TG) significantly decreased. Although prostanoids did not show significant change, changes in T-cho were correlated with changes in Dinor and changes in Iso. These results suggest that PGI2 and TXA2 of systemic origin might be related to the pathophysiology of hypertension and hyperlipidemia and that the dynamics of PGI2, TXA2 and F2-isoprostanes might be related to not only blood pressure regulation but also lipid and glucose metabolism. |
doi_str_mv | 10.1016/S0162-3109(99)00137-X |
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These results suggest that PGI2 and TXA2 of systemic origin might be related to the pathophysiology of hypertension and hyperlipidemia and that the dynamics of PGI2, TXA2 and F2-isoprostanes might be related to not only blood pressure regulation but also lipid and glucose metabolism.</description><identifier>ISSN: 0162-3109</identifier><identifier>DOI: 10.1016/S0162-3109(99)00137-X</identifier><identifier>PMID: 10604544</identifier><identifier>CODEN: IMMUDP</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Arterial hypertension. Arterial hypotension ; Aspirin - pharmacology ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Dinoprost - metabolism ; Dipyridamole - pharmacology ; Eicosapentaenoic acid ; Eicosapentaenoic Acid - pharmacology ; Epoprostenol - metabolism ; F2-isoprostane ; Humans ; Hyperlipidemia ; Hyperlipidemias - metabolism ; Hypertension ; Hypertension - metabolism ; Medical sciences ; Platelet Aggregation Inhibitors - pharmacology ; Prostacyclin ; Thromboxane A2 ; Thromboxane A2 - metabolism ; Ticlopidine - pharmacology</subject><ispartof>Immunopharmacology, 1999-10, Vol.44 (1-2), p.193-198</ispartof><rights>1999 Elsevier Science B.V.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c305t-8e247dd865f61644f72ba8c165a78656059e3d2f2125126593628608b82241b3</citedby><cites>FETCH-LOGICAL-c305t-8e247dd865f61644f72ba8c165a78656059e3d2f2125126593628608b82241b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1210339$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10604544$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamada, Masaaki</creatorcontrib><creatorcontrib>Omata, Ken</creatorcontrib><creatorcontrib>Abe, Fumiaki</creatorcontrib><creatorcontrib>Ito, Sadayoshi</creatorcontrib><creatorcontrib>Keishi Abe</creatorcontrib><title>Changes in prostacyclin, thromboxane A2 and F2-isoprostanes, and influence of eicosapentaenoic acid and antiplatelet agents in patients with hypertension and hyperlipidemia</title><title>Immunopharmacology</title><addtitle>Immunopharmacology</addtitle><description>Prostacyclin (PGI2), thromboxane A2 (TXA2) and F2-isoprostanes, prostaglandin F2-like compounds, have wide and contrasting spectrum of biological activities and may influence blood pressure and atherogenesis. To investigate the dynamics of PGI2, TXA2 and F2-isoprostanes in patients with hypertension and hyperlipidemia (HH group), we measured the major urinary metabolites of PGI2: 6-keto PGF1α (Keto) and 2,3-dinor-6-keto PGF1α (Dinor), those of TXA2: TXB2 and 11-dehydro TXB2 (Dehydro), and urinary 8-isoprostane (Iso) in 34 patients. Urinary excretion of Dinor was significantly lower in patients than in controls and that of Dehydro was significantly higher in patients than in controls. Keto, TXB2 and Iso were not significantly different between them. Antiplatelet agents decreased not only TXA2 metabolites but also PGI2 metabolites. Urinary C-peptide immunoreactivity was correlated with Dinor and Dehydro. After administration of eicosapentaenoic acid (EPA), total cholesterol (T-cho) and triglycerides (TG) significantly decreased. Although prostanoids did not show significant change, changes in T-cho were correlated with changes in Dinor and changes in Iso. These results suggest that PGI2 and TXA2 of systemic origin might be related to the pathophysiology of hypertension and hyperlipidemia and that the dynamics of PGI2, TXA2 and F2-isoprostanes might be related to not only blood pressure regulation but also lipid and glucose metabolism.</description><subject>Arterial hypertension. Arterial hypotension</subject><subject>Aspirin - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Dinoprost - metabolism</subject><subject>Dipyridamole - pharmacology</subject><subject>Eicosapentaenoic acid</subject><subject>Eicosapentaenoic Acid - pharmacology</subject><subject>Epoprostenol - metabolism</subject><subject>F2-isoprostane</subject><subject>Humans</subject><subject>Hyperlipidemia</subject><subject>Hyperlipidemias - metabolism</subject><subject>Hypertension</subject><subject>Hypertension - metabolism</subject><subject>Medical sciences</subject><subject>Platelet Aggregation Inhibitors - pharmacology</subject><subject>Prostacyclin</subject><subject>Thromboxane A2</subject><subject>Thromboxane A2 - metabolism</subject><subject>Ticlopidine - pharmacology</subject><issn>0162-3109</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNqFkc1u1DAUhbMA0dLyCCAvECpSA7YTO8kKVSMKlSqxoIvurBvnpnNRYofYQ5l34iHxJCNgx8a2jr7j-3Oy7KXg7wQX-v3XdMi8ELy5aJq3nIuiyu-fZKd_5JPseQjfOOdl1ahn2YngmpeqLE-zX5stuAcMjBybZh8i2L0dyF2yuJ392Pqf4JBdSQauY9cyp-BXzGG4XERy_bBDZ5H5niFZH2BCFwGdJ8vAUrdg4CJNA0QcMDJ4SMRaEyIt70eKW7bdTzhHdIG8W1yLMNBEHY4E59nTHoaAL473WXZ3_fFu8zm__fLpZnN1m9uCq5jXKMuq62qtei10WfaVbKG2Qiuokqi5arDoZC-FVEJq1RRa1prXbS1lKdriLHuzfpsm_b7DEM1IweIwpKH9LhidDFoVIoFqBW1aSZixN9NMI8x7I7g5JGOWZMwhAtM0ZknG3Cffq2OBXTti949rjSUBr48ABAtDP4OzFP5yUvCiaBL2YcUwLeMH4WyCpUMUHc1oo-k8_aeT33jLrx8</recordid><startdate>19991015</startdate><enddate>19991015</enddate><creator>Yamada, Masaaki</creator><creator>Omata, Ken</creator><creator>Abe, Fumiaki</creator><creator>Ito, Sadayoshi</creator><creator>Keishi Abe</creator><general>Elsevier B.V</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>19991015</creationdate><title>Changes in prostacyclin, thromboxane A2 and F2-isoprostanes, and influence of eicosapentaenoic acid and antiplatelet agents in patients with hypertension and hyperlipidemia</title><author>Yamada, Masaaki ; Omata, Ken ; Abe, Fumiaki ; Ito, Sadayoshi ; Keishi Abe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c305t-8e247dd865f61644f72ba8c165a78656059e3d2f2125126593628608b82241b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Arterial hypertension. Arterial hypotension</topic><topic>Aspirin - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Dinoprost - metabolism</topic><topic>Dipyridamole - pharmacology</topic><topic>Eicosapentaenoic acid</topic><topic>Eicosapentaenoic Acid - pharmacology</topic><topic>Epoprostenol - metabolism</topic><topic>F2-isoprostane</topic><topic>Humans</topic><topic>Hyperlipidemia</topic><topic>Hyperlipidemias - metabolism</topic><topic>Hypertension</topic><topic>Hypertension - metabolism</topic><topic>Medical sciences</topic><topic>Platelet Aggregation Inhibitors - pharmacology</topic><topic>Prostacyclin</topic><topic>Thromboxane A2</topic><topic>Thromboxane A2 - metabolism</topic><topic>Ticlopidine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamada, Masaaki</creatorcontrib><creatorcontrib>Omata, Ken</creatorcontrib><creatorcontrib>Abe, Fumiaki</creatorcontrib><creatorcontrib>Ito, Sadayoshi</creatorcontrib><creatorcontrib>Keishi Abe</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>MEDLINE - Academic</collection><jtitle>Immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamada, Masaaki</au><au>Omata, Ken</au><au>Abe, Fumiaki</au><au>Ito, Sadayoshi</au><au>Keishi Abe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in prostacyclin, thromboxane A2 and F2-isoprostanes, and influence of eicosapentaenoic acid and antiplatelet agents in patients with hypertension and hyperlipidemia</atitle><jtitle>Immunopharmacology</jtitle><addtitle>Immunopharmacology</addtitle><date>1999-10-15</date><risdate>1999</risdate><volume>44</volume><issue>1-2</issue><spage>193</spage><epage>198</epage><pages>193-198</pages><issn>0162-3109</issn><coden>IMMUDP</coden><abstract>Prostacyclin (PGI2), thromboxane A2 (TXA2) and F2-isoprostanes, prostaglandin F2-like compounds, have wide and contrasting spectrum of biological activities and may influence blood pressure and atherogenesis. To investigate the dynamics of PGI2, TXA2 and F2-isoprostanes in patients with hypertension and hyperlipidemia (HH group), we measured the major urinary metabolites of PGI2: 6-keto PGF1α (Keto) and 2,3-dinor-6-keto PGF1α (Dinor), those of TXA2: TXB2 and 11-dehydro TXB2 (Dehydro), and urinary 8-isoprostane (Iso) in 34 patients. Urinary excretion of Dinor was significantly lower in patients than in controls and that of Dehydro was significantly higher in patients than in controls. Keto, TXB2 and Iso were not significantly different between them. Antiplatelet agents decreased not only TXA2 metabolites but also PGI2 metabolites. Urinary C-peptide immunoreactivity was correlated with Dinor and Dehydro. After administration of eicosapentaenoic acid (EPA), total cholesterol (T-cho) and triglycerides (TG) significantly decreased. Although prostanoids did not show significant change, changes in T-cho were correlated with changes in Dinor and changes in Iso. These results suggest that PGI2 and TXA2 of systemic origin might be related to the pathophysiology of hypertension and hyperlipidemia and that the dynamics of PGI2, TXA2 and F2-isoprostanes might be related to not only blood pressure regulation but also lipid and glucose metabolism.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10604544</pmid><doi>10.1016/S0162-3109(99)00137-X</doi><tpages>6</tpages></addata></record> |
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subjects | Arterial hypertension. Arterial hypotension Aspirin - pharmacology Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Dinoprost - metabolism Dipyridamole - pharmacology Eicosapentaenoic acid Eicosapentaenoic Acid - pharmacology Epoprostenol - metabolism F2-isoprostane Humans Hyperlipidemia Hyperlipidemias - metabolism Hypertension Hypertension - metabolism Medical sciences Platelet Aggregation Inhibitors - pharmacology Prostacyclin Thromboxane A2 Thromboxane A2 - metabolism Ticlopidine - pharmacology |
title | Changes in prostacyclin, thromboxane A2 and F2-isoprostanes, and influence of eicosapentaenoic acid and antiplatelet agents in patients with hypertension and hyperlipidemia |
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