Thromboxane A2 Receptor Antagonism and Synthase Inhibition in Essential Hypertension
Short-term effects of ridogrel, a combined thromboxane synthase inhibitor and receptor antagonist, were investigated in 16 patients with uncomplicated essential hypertension. After a 2-week placebo period without antihypertensive medication, patients were admitted to the hospital overnight on two oc...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 1993-08, Vol.22 (2), p.197-203 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Ritter, James M Barrow, Susan E Doktor, Hilary S Stratton, Paula D Edwards, Jacqueline S Henry, John A Gould, Susan |
| description | Short-term effects of ridogrel, a combined thromboxane synthase inhibitor and receptor antagonist, were investigated in 16 patients with uncomplicated essential hypertension. After a 2-week placebo period without antihypertensive medication, patients were admitted to the hospital overnight on two occasions 3 weeks apart On each occasion, they received two doses of either placebo or ridogrel (300 mg) 12 hours apart according to a double-blind crossover protocol. Renal and systemic thromboxane A2 and prostacyclin biosynthesis were investigated by measuring urinary excretion of thromboxane B2, 6-oxoprostaglandin F1α, and their respective 2,3-dinor metabolites using gas chromatography/mass spectrometry. Responses of platelets to a thromboxane A2 mimetic and to adenosine diphosphate were studied turbidometrically. Blood pressure was measured automatically at 20-minute intervals. Ridogrel reduced excretion of 2,3-dinor-thromboxane B2 and thromboxane B2 compared with placebo (21±6 versus 279±28 and 14±4 versus 39±9 ng/g creatinine, respectively, P |
| doi_str_mv | 10.1161/01.hyp.22.2.197 |
| format | Article |
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After a 2-week placebo period without antihypertensive medication, patients were admitted to the hospital overnight on two occasions 3 weeks apart On each occasion, they received two doses of either placebo or ridogrel (300 mg) 12 hours apart according to a double-blind crossover protocol. Renal and systemic thromboxane A2 and prostacyclin biosynthesis were investigated by measuring urinary excretion of thromboxane B2, 6-oxoprostaglandin F1α, and their respective 2,3-dinor metabolites using gas chromatography/mass spectrometry. Responses of platelets to a thromboxane A2 mimetic and to adenosine diphosphate were studied turbidometrically. Blood pressure was measured automatically at 20-minute intervals. Ridogrel reduced excretion of 2,3-dinor-thromboxane B2 and thromboxane B2 compared with placebo (21±6 versus 279±28 and 14±4 versus 39±9 ng/g creatinine, respectively, P<.0001 and P<.05). Excretion of 2,3-dinor-6- oxoprostaglandin F1α and 6-oxoprostaglandin F1α, was increased by ridogrel compared with placebo (184±20 versus 146±11 and 86±9 versus 58±6 ng/g creatinine, respectively; P<.05). Ridogrel selectively antagonized platelet aggregation to the thromboxane mimetic (P<.0001). Blood pressure did not differ significantly between ridogrel and placebo treatment periods. Thus, in patients with essential hypertension, acute administration of ridogrel reduces renal and extrarenal thromboxane A2 biosynthesis, increases renal and extrarenal prostacyclin biosynthesis, inhibits thromboxane receptor-activated platelet aggregation, but has no effect on systemic arterial pressure.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.22.2.197</identifier><identifier>PMID: 8340155</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Adult ; Aged ; Antihypertensive agents ; Biological and medical sciences ; Blood Pressure - drug effects ; Cardiovascular system ; Double-Blind Method ; Eicosanoids - urine ; Female ; Humans ; Hypertension - drug therapy ; Hypertension - metabolism ; Hypertension - physiopathology ; Male ; Medical sciences ; Middle Aged ; Pentanoic Acids - blood ; Pentanoic Acids - therapeutic use ; Pharmacology. Drug treatments ; Platelet Aggregation - drug effects ; Platelet Aggregation Inhibitors - therapeutic use ; Pyridines - blood ; Pyridines - therapeutic use ; Receptors, Thromboxane - antagonists & inhibitors ; Thromboxane B2 - blood ; Thromboxane-A Synthase - antagonists & inhibitors</subject><ispartof>Hypertension (Dallas, Tex. 1979), 1993-08, Vol.22 (2), p.197-203</ispartof><rights>1993 American Heart Association, Inc.</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5149-e7a6f8a979bff9727adfabf0bb356795861a55589f5da7590ea9566e368de8943</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4833357$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8340155$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ritter, James M</creatorcontrib><creatorcontrib>Barrow, Susan E</creatorcontrib><creatorcontrib>Doktor, Hilary S</creatorcontrib><creatorcontrib>Stratton, Paula D</creatorcontrib><creatorcontrib>Edwards, Jacqueline S</creatorcontrib><creatorcontrib>Henry, John A</creatorcontrib><creatorcontrib>Gould, Susan</creatorcontrib><title>Thromboxane A2 Receptor Antagonism and Synthase Inhibition in Essential Hypertension</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Short-term effects of ridogrel, a combined thromboxane synthase inhibitor and receptor antagonist, were investigated in 16 patients with uncomplicated essential hypertension. After a 2-week placebo period without antihypertensive medication, patients were admitted to the hospital overnight on two occasions 3 weeks apart On each occasion, they received two doses of either placebo or ridogrel (300 mg) 12 hours apart according to a double-blind crossover protocol. Renal and systemic thromboxane A2 and prostacyclin biosynthesis were investigated by measuring urinary excretion of thromboxane B2, 6-oxoprostaglandin F1α, and their respective 2,3-dinor metabolites using gas chromatography/mass spectrometry. Responses of platelets to a thromboxane A2 mimetic and to adenosine diphosphate were studied turbidometrically. Blood pressure was measured automatically at 20-minute intervals. Ridogrel reduced excretion of 2,3-dinor-thromboxane B2 and thromboxane B2 compared with placebo (21±6 versus 279±28 and 14±4 versus 39±9 ng/g creatinine, respectively, P<.0001 and P<.05). Excretion of 2,3-dinor-6- oxoprostaglandin F1α and 6-oxoprostaglandin F1α, was increased by ridogrel compared with placebo (184±20 versus 146±11 and 86±9 versus 58±6 ng/g creatinine, respectively; P<.05). Ridogrel selectively antagonized platelet aggregation to the thromboxane mimetic (P<.0001). Blood pressure did not differ significantly between ridogrel and placebo treatment periods. Thus, in patients with essential hypertension, acute administration of ridogrel reduces renal and extrarenal thromboxane A2 biosynthesis, increases renal and extrarenal prostacyclin biosynthesis, inhibits thromboxane receptor-activated platelet aggregation, but has no effect on systemic arterial pressure.</description><subject>Adult</subject><subject>Aged</subject><subject>Antihypertensive agents</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiovascular system</subject><subject>Double-Blind Method</subject><subject>Eicosanoids - urine</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pentanoic Acids - blood</subject><subject>Pentanoic Acids - therapeutic use</subject><subject>Pharmacology. Drug treatments</subject><subject>Platelet Aggregation - drug effects</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Pyridines - blood</subject><subject>Pyridines - therapeutic use</subject><subject>Receptors, Thromboxane - antagonists & inhibitors</subject><subject>Thromboxane B2 - blood</subject><subject>Thromboxane-A Synthase - antagonists & inhibitors</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kM2LFDEQxYMo67h69iTkIN66N5-d5Dgsq7OwoOgIegrp7ord2p20SQ_r_PdmmGHrUlS9Xz2oh9BbSmpKG3pDaD0cl5qxmtXUqGdoQyUTlZANf442hBpRGUp_vESvcv5NCBVCqCt0pbkgVMoN2u-HFOc2_nMB8Jbhr9DBssaEt2F1v2IY84xd6PG3Y1gHlwHfh2Fsx3WMAY8B3-UMYR3dhHfHBdIKIRflNXrh3ZThzaVfo-8f7_a3u-rh86f72-1D1UkqTAXKNV47o0zrvVFMud671pO25bJRRuqGOimlNl72TklDwBnZNMAb3YM2gl-jD2ffJcW_B8irncfcwTSVZ-IhWyW1KgeygDdnsEsx5wTeLmmcXTpaSuwpR0uo3f38YhmzzJYcy8W7i_WhnaF_4i_BFf39RXe5c5NPLnRjfsKE5pzLk404Y49xWiHlP9PhEZIdwE3rYEkpwRpdUWM40WWqTivD_wNnzIsd</recordid><startdate>199308</startdate><enddate>199308</enddate><creator>Ritter, James M</creator><creator>Barrow, Susan E</creator><creator>Doktor, Hilary S</creator><creator>Stratton, Paula D</creator><creator>Edwards, Jacqueline S</creator><creator>Henry, John A</creator><creator>Gould, Susan</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>7X8</scope></search><sort><creationdate>199308</creationdate><title>Thromboxane A2 Receptor Antagonism and Synthase Inhibition in Essential Hypertension</title><author>Ritter, James M ; Barrow, Susan E ; Doktor, Hilary S ; Stratton, Paula D ; Edwards, Jacqueline S ; Henry, John A ; Gould, Susan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5149-e7a6f8a979bff9727adfabf0bb356795861a55589f5da7590ea9566e368de8943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antihypertensive agents</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiovascular system</topic><topic>Double-Blind Method</topic><topic>Eicosanoids - urine</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pentanoic Acids - blood</topic><topic>Pentanoic Acids - therapeutic use</topic><topic>Pharmacology. Drug treatments</topic><topic>Platelet Aggregation - drug effects</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Pyridines - blood</topic><topic>Pyridines - therapeutic use</topic><topic>Receptors, Thromboxane - antagonists & inhibitors</topic><topic>Thromboxane B2 - blood</topic><topic>Thromboxane-A Synthase - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ritter, James M</creatorcontrib><creatorcontrib>Barrow, Susan E</creatorcontrib><creatorcontrib>Doktor, Hilary S</creatorcontrib><creatorcontrib>Stratton, Paula D</creatorcontrib><creatorcontrib>Edwards, Jacqueline S</creatorcontrib><creatorcontrib>Henry, John A</creatorcontrib><creatorcontrib>Gould, Susan</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>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ritter, James M</au><au>Barrow, Susan E</au><au>Doktor, Hilary S</au><au>Stratton, Paula D</au><au>Edwards, Jacqueline S</au><au>Henry, John A</au><au>Gould, Susan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thromboxane A2 Receptor Antagonism and Synthase Inhibition in Essential Hypertension</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>1993-08</date><risdate>1993</risdate><volume>22</volume><issue>2</issue><spage>197</spage><epage>203</epage><pages>197-203</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Short-term effects of ridogrel, a combined thromboxane synthase inhibitor and receptor antagonist, were investigated in 16 patients with uncomplicated essential hypertension. After a 2-week placebo period without antihypertensive medication, patients were admitted to the hospital overnight on two occasions 3 weeks apart On each occasion, they received two doses of either placebo or ridogrel (300 mg) 12 hours apart according to a double-blind crossover protocol. Renal and systemic thromboxane A2 and prostacyclin biosynthesis were investigated by measuring urinary excretion of thromboxane B2, 6-oxoprostaglandin F1α, and their respective 2,3-dinor metabolites using gas chromatography/mass spectrometry. Responses of platelets to a thromboxane A2 mimetic and to adenosine diphosphate were studied turbidometrically. Blood pressure was measured automatically at 20-minute intervals. Ridogrel reduced excretion of 2,3-dinor-thromboxane B2 and thromboxane B2 compared with placebo (21±6 versus 279±28 and 14±4 versus 39±9 ng/g creatinine, respectively, P<.0001 and P<.05). Excretion of 2,3-dinor-6- oxoprostaglandin F1α and 6-oxoprostaglandin F1α, was increased by ridogrel compared with placebo (184±20 versus 146±11 and 86±9 versus 58±6 ng/g creatinine, respectively; P<.05). Ridogrel selectively antagonized platelet aggregation to the thromboxane mimetic (P<.0001). Blood pressure did not differ significantly between ridogrel and placebo treatment periods. Thus, in patients with essential hypertension, acute administration of ridogrel reduces renal and extrarenal thromboxane A2 biosynthesis, increases renal and extrarenal prostacyclin biosynthesis, inhibits thromboxane receptor-activated platelet aggregation, but has no effect on systemic arterial pressure.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>8340155</pmid><doi>10.1161/01.hyp.22.2.197</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hypertension (Dallas, Tex. 1979), 1993-08, Vol.22 (2), p.197-203 |
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| source | MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals; Journals@Ovid Complete |
| subjects | Adult Aged Antihypertensive agents Biological and medical sciences Blood Pressure - drug effects Cardiovascular system Double-Blind Method Eicosanoids - urine Female Humans Hypertension - drug therapy Hypertension - metabolism Hypertension - physiopathology Male Medical sciences Middle Aged Pentanoic Acids - blood Pentanoic Acids - therapeutic use Pharmacology. Drug treatments Platelet Aggregation - drug effects Platelet Aggregation Inhibitors - therapeutic use Pyridines - blood Pyridines - therapeutic use Receptors, Thromboxane - antagonists & inhibitors Thromboxane B2 - blood Thromboxane-A Synthase - antagonists & inhibitors |
| title | Thromboxane A2 Receptor Antagonism and Synthase Inhibition in Essential Hypertension |
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