Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan
Structural and functional alterations of the vasculature may contribute to complications of hypertension. Because angiotensin II may be pivotal in some of these vascular abnormalities, we tested the hypothesis that the angiotensin type 1 (AT(1)) receptor antagonist losartan, in contrast to the beta-...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2000-04, Vol.101 (14), p.1653-1659 |
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| creator | SCHIFFRIN, E. L JEONG BAE PARK INTENGAN, H. D TOUYZ, R. M |
| description | Structural and functional alterations of the vasculature may contribute to complications of hypertension. Because angiotensin II may be pivotal in some of these vascular abnormalities, we tested the hypothesis that the angiotensin type 1 (AT(1)) receptor antagonist losartan, in contrast to the beta-blocker atenolol, would correct resistance artery abnormalities in patients with essential hypertension.
Nineteen untreated patients with mild essential hypertension (47+/-2 years, range 30 to 65 years; 57% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for 1 year. Nine age/sex-matched normotensive subjects were also studied. Both treatments reduced blood pressure to a comparable degree (losartan, from 149+/-4.1/101+/-1.6 to 128+/-3.6/86+/-2.2 mm Hg, P |
| doi_str_mv | 10.1161/01.cir.101.14.1653 |
| format | Article |
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Nineteen untreated patients with mild essential hypertension (47+/-2 years, range 30 to 65 years; 57% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for 1 year. Nine age/sex-matched normotensive subjects were also studied. Both treatments reduced blood pressure to a comparable degree (losartan, from 149+/-4.1/101+/-1.6 to 128+/-3.6/86+/-2.2 mm Hg, P<0.01; atenolol, from 150+/-4.0/99+/-1.2 to 130+/-3.2/84+/-1.4 mm Hg, P<0.01). Resistance arteries (luminal diameter 150 to 350 microm) dissected from gluteal subcutaneous biopsies were studied on a pressurized myograph. After 1 year of treatment, the ratio of the media width to lumen diameter of arteries from losartan-treated patients was significantly reduced (from 8.4+/-0.4% to 6.7+/-0.3%, P<0.01). Arteries from atenolol-treated patients exhibited no significant change (from 8. 3+/-0.3% to 8.8+/-0.5% after treatment). Endothelium-dependent relaxation (acetylcholine-induced) was normalized by losartan (from 82.1+/-4.9% to 94.7+/-1.1%, P<0.01) but not by atenolol (from 80. 4+/-2.7% to 81.7+/-4.6%). Endothelium-independent relaxation (by sodium nitroprusside) was unchanged after treatment.
The AT(1) antagonist losartan corrected the altered structure and endothelial dysfunction of resistance arteries from patients with essential hypertension, whereas the beta-blocker atenolol had no effect.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.101.14.1653</identifier><identifier>PMID: 10758046</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Acetylcholine - pharmacology ; Adult ; Angiotensin Receptor Antagonists ; Antihypertensive agents ; Antihypertensive Agents - therapeutic use ; Arteries - drug effects ; Arteries - pathology ; Arteries - physiopathology ; Atenolol - therapeutic use ; Biological and medical sciences ; Buttocks - blood supply ; Cardiovascular system ; Double-Blind Method ; Endothelium, Vascular - physiopathology ; Female ; Humans ; Hypertension - drug therapy ; Hypertension - pathology ; Hypertension - physiopathology ; Losartan - therapeutic use ; Male ; Medical sciences ; Middle Aged ; Pharmacology. Drug treatments ; Receptor, Angiotensin, Type 1 ; Receptor, Angiotensin, Type 2 ; Space life sciences ; Vascular Resistance ; Vasodilation</subject><ispartof>Circulation (New York, N.Y.), 2000-04, Vol.101 (14), p.1653-1659</ispartof><rights>2000 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Apr 11, 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-dc4ec6c2f134b205f271f2f886510bfaaced9f0562774423338c9779e9ad1f123</citedby><cites>FETCH-LOGICAL-c508t-dc4ec6c2f134b205f271f2f886510bfaaced9f0562774423338c9779e9ad1f123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1323230$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10758046$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SCHIFFRIN, E. L</creatorcontrib><creatorcontrib>JEONG BAE PARK</creatorcontrib><creatorcontrib>INTENGAN, H. D</creatorcontrib><creatorcontrib>TOUYZ, R. M</creatorcontrib><title>Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Structural and functional alterations of the vasculature may contribute to complications of hypertension. Because angiotensin II may be pivotal in some of these vascular abnormalities, we tested the hypothesis that the angiotensin type 1 (AT(1)) receptor antagonist losartan, in contrast to the beta-blocker atenolol, would correct resistance artery abnormalities in patients with essential hypertension.
Nineteen untreated patients with mild essential hypertension (47+/-2 years, range 30 to 65 years; 57% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for 1 year. Nine age/sex-matched normotensive subjects were also studied. Both treatments reduced blood pressure to a comparable degree (losartan, from 149+/-4.1/101+/-1.6 to 128+/-3.6/86+/-2.2 mm Hg, P<0.01; atenolol, from 150+/-4.0/99+/-1.2 to 130+/-3.2/84+/-1.4 mm Hg, P<0.01). Resistance arteries (luminal diameter 150 to 350 microm) dissected from gluteal subcutaneous biopsies were studied on a pressurized myograph. After 1 year of treatment, the ratio of the media width to lumen diameter of arteries from losartan-treated patients was significantly reduced (from 8.4+/-0.4% to 6.7+/-0.3%, P<0.01). Arteries from atenolol-treated patients exhibited no significant change (from 8. 3+/-0.3% to 8.8+/-0.5% after treatment). Endothelium-dependent relaxation (acetylcholine-induced) was normalized by losartan (from 82.1+/-4.9% to 94.7+/-1.1%, P<0.01) but not by atenolol (from 80. 4+/-2.7% to 81.7+/-4.6%). Endothelium-independent relaxation (by sodium nitroprusside) was unchanged after treatment.
The AT(1) antagonist losartan corrected the altered structure and endothelial dysfunction of resistance arteries from patients with essential hypertension, whereas the beta-blocker atenolol had no effect.</description><subject>Acetylcholine - pharmacology</subject><subject>Adult</subject><subject>Angiotensin Receptor Antagonists</subject><subject>Antihypertensive agents</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Arteries - drug effects</subject><subject>Arteries - pathology</subject><subject>Arteries - physiopathology</subject><subject>Atenolol - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Buttocks - blood supply</subject><subject>Cardiovascular system</subject><subject>Double-Blind Method</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - pathology</subject><subject>Hypertension - physiopathology</subject><subject>Losartan - therapeutic use</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pharmacology. Drug treatments</subject><subject>Receptor, Angiotensin, Type 1</subject><subject>Receptor, Angiotensin, Type 2</subject><subject>Space life sciences</subject><subject>Vascular Resistance</subject><subject>Vasodilation</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1qWzEQhUVpaZy0L9BFESVkd12Nfu7Pspi0DQQKoV0LWXcUK1xLrqS78DvkoaNbG1qKFsPM-c4ZwRDyAdgaoIXPDNbWpzXUCnINrRKvyAoUl41UYnhNVoyxoekE5xfkMuen2raiU2_JBbBO9Uy2K_K8iSmhLT4GGh01qWDyZqK5pNmWOSE1YaQYxlh2OC3KeMxuDieHD3Q3702gmDOGssi74wFrSMiLvj3SaqsRjz7-mQVal-GhxFSHxTzG4HOhU8x1sQnvyBtnpozvz_WK_Pp6-3Pzvbn_8e1u8-W-sYr1pRmtRNta7kDILWfK8Q4cd33fKmBbZ4zFcXBMtbzrpORCiN4OXTfgYEZwwMUVuTnlHlL8PWMueu-zxWkyAeOcdQdMCMlVBT_9Bz7FOYX6N82BtwPA0FeInyCbYs4JnT4kvzfpqIHp5VCagd7cPdQWNEi9HKqaPp6T5-0ex38sp8tU4PoMmGzN5JIJ1ue_nOD1MfECCIee2w</recordid><startdate>20000411</startdate><enddate>20000411</enddate><creator>SCHIFFRIN, E. L</creator><creator>JEONG BAE PARK</creator><creator>INTENGAN, H. D</creator><creator>TOUYZ, R. M</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20000411</creationdate><title>Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan</title><author>SCHIFFRIN, E. L ; JEONG BAE PARK ; INTENGAN, H. D ; TOUYZ, R. M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-dc4ec6c2f134b205f271f2f886510bfaaced9f0562774423338c9779e9ad1f123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Adult</topic><topic>Angiotensin Receptor Antagonists</topic><topic>Antihypertensive agents</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Arteries - drug effects</topic><topic>Arteries - pathology</topic><topic>Arteries - physiopathology</topic><topic>Atenolol - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Buttocks - blood supply</topic><topic>Cardiovascular system</topic><topic>Double-Blind Method</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - pathology</topic><topic>Hypertension - physiopathology</topic><topic>Losartan - therapeutic use</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pharmacology. Drug treatments</topic><topic>Receptor, Angiotensin, Type 1</topic><topic>Receptor, Angiotensin, Type 2</topic><topic>Space life sciences</topic><topic>Vascular Resistance</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SCHIFFRIN, E. L</creatorcontrib><creatorcontrib>JEONG BAE PARK</creatorcontrib><creatorcontrib>INTENGAN, H. D</creatorcontrib><creatorcontrib>TOUYZ, R. M</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>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SCHIFFRIN, E. L</au><au>JEONG BAE PARK</au><au>INTENGAN, H. D</au><au>TOUYZ, R. M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2000-04-11</date><risdate>2000</risdate><volume>101</volume><issue>14</issue><spage>1653</spage><epage>1659</epage><pages>1653-1659</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Structural and functional alterations of the vasculature may contribute to complications of hypertension. Because angiotensin II may be pivotal in some of these vascular abnormalities, we tested the hypothesis that the angiotensin type 1 (AT(1)) receptor antagonist losartan, in contrast to the beta-blocker atenolol, would correct resistance artery abnormalities in patients with essential hypertension.
Nineteen untreated patients with mild essential hypertension (47+/-2 years, range 30 to 65 years; 57% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for 1 year. Nine age/sex-matched normotensive subjects were also studied. Both treatments reduced blood pressure to a comparable degree (losartan, from 149+/-4.1/101+/-1.6 to 128+/-3.6/86+/-2.2 mm Hg, P<0.01; atenolol, from 150+/-4.0/99+/-1.2 to 130+/-3.2/84+/-1.4 mm Hg, P<0.01). Resistance arteries (luminal diameter 150 to 350 microm) dissected from gluteal subcutaneous biopsies were studied on a pressurized myograph. After 1 year of treatment, the ratio of the media width to lumen diameter of arteries from losartan-treated patients was significantly reduced (from 8.4+/-0.4% to 6.7+/-0.3%, P<0.01). Arteries from atenolol-treated patients exhibited no significant change (from 8. 3+/-0.3% to 8.8+/-0.5% after treatment). Endothelium-dependent relaxation (acetylcholine-induced) was normalized by losartan (from 82.1+/-4.9% to 94.7+/-1.1%, P<0.01) but not by atenolol (from 80. 4+/-2.7% to 81.7+/-4.6%). Endothelium-independent relaxation (by sodium nitroprusside) was unchanged after treatment.
The AT(1) antagonist losartan corrected the altered structure and endothelial dysfunction of resistance arteries from patients with essential hypertension, whereas the beta-blocker atenolol had no effect.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>10758046</pmid><doi>10.1161/01.cir.101.14.1653</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Acetylcholine - pharmacology Adult Angiotensin Receptor Antagonists Antihypertensive agents Antihypertensive Agents - therapeutic use Arteries - drug effects Arteries - pathology Arteries - physiopathology Atenolol - therapeutic use Biological and medical sciences Buttocks - blood supply Cardiovascular system Double-Blind Method Endothelium, Vascular - physiopathology Female Humans Hypertension - drug therapy Hypertension - pathology Hypertension - physiopathology Losartan - therapeutic use Male Medical sciences Middle Aged Pharmacology. Drug treatments Receptor, Angiotensin, Type 1 Receptor, Angiotensin, Type 2 Space life sciences Vascular Resistance Vasodilation |
| title | Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan |
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