Acute Endothelin-Receptor Inhibition Does Not Attenuate Acetylcholine-Induced Coronary Vasoconstriction in Experimental Hypercholesterolemia
Endothelin (ET) may mediate the enhanced coronary vasoconstriction associated with hypercholesterolemia. We hypothesized that short-term inhibition of ET receptors attenuates the coronary epicardial vasoconstrictor response to acetylcholine in experimental hypercholesterolemia. ET-1 (group I, n = 5;...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 1998-01, Vol.18 (1), p.108-113 |
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| creator | Hasdai, David Best, Patricia J.M Cannan, Charles R Mathew, Verghese Schwartz, Robert S Holmes, David R. Jr Lerman, Amir |
| description | Endothelin (ET) may mediate the enhanced coronary vasoconstriction associated with hypercholesterolemia. We hypothesized that short-term inhibition of ET receptors attenuates the coronary epicardial vasoconstrictor response to acetylcholine in experimental hypercholesterolemia. ET-1 (group I, n = 5; 5 ng [center dot] kg [center dot] min) and acetylcholine (group III, n = 7; 10 to 10 mol/L) were given by intracoronary infusion in pigs. ET-1 and acetylcholine were also infused with the specific ETA-receptor blocker FR-139317 (5 micro gram [center dot] kg [center dot] min (); group II, n = 6; group IV, n = 6). Acetylcholine was also infused with the combined ET-receptor blocker, bosentan (0.5 mg/kg plus 1 mg [center dot] kg [center dot] h, group V, n = 5). The ETB-receptor agonist sarafotoxin 6c (5 ng [center dot] kg [center dot] min; n = 4) was also infused. The percentage change in coronary artery diameter (%Delta CAD) to the infusions was measured at baseline and after 10 weeks of high-cholesterol diet in all animals. Sarafotoxin 6c mildly reduced %Delta CAD at baseline and 10 weeks (-10 +/- 2% and -12 +/- 3%, respectively). FR-139317 did not attenuate the epicardial vasoconstrictor response to ET-1 at baseline (%Delta CAD -18 +/- 8% for group I versus -12 +/- 6% for group II; P = NS) but did at 10 weeks (%Delta CAD) -77 +/- 14% for group I versus -14 +/- 6% for group II; P < .05). FR-139317 did not affect the response to acetylcholine at baseline (%Delta CAD 5 +/- 2% for group III versus 7 +/- 3% for group IV, P = NS) or at 10 weeks (%Delta CAD -23 +/- 12% for group III versus -19 +/- 7% for group IV; P = NS). Bosentan did not affect the response to acetylcholine at baseline or 10 weeks. Short-term ET-receptor inhibition in experimental hypercholesterolemia attenuated the enhanced coronary epicardial vasoconstrictor effects of ET-1 but not acetylcholine-induced coronary epicardial vasoconstriction, suggesting that acetylcholine-induced coronary epicardial vasoconstriction may not be mediated by ET receptors. (Arterioscler Thromb Vasc Biol. 1998;18:108-113.) |
| doi_str_mv | 10.1161/01.ATV.18.1.108 |
| format | Article |
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Jr ; Lerman, Amir</creator><creatorcontrib>Hasdai, David ; Best, Patricia J.M ; Cannan, Charles R ; Mathew, Verghese ; Schwartz, Robert S ; Holmes, David R. Jr ; Lerman, Amir</creatorcontrib><description>Endothelin (ET) may mediate the enhanced coronary vasoconstriction associated with hypercholesterolemia. We hypothesized that short-term inhibition of ET receptors attenuates the coronary epicardial vasoconstrictor response to acetylcholine in experimental hypercholesterolemia. ET-1 (group I, n = 5; 5 ng [center dot] kg [center dot] min) and acetylcholine (group III, n = 7; 10 to 10 mol/L) were given by intracoronary infusion in pigs. ET-1 and acetylcholine were also infused with the specific ETA-receptor blocker FR-139317 (5 micro gram [center dot] kg [center dot] min (); group II, n = 6; group IV, n = 6). Acetylcholine was also infused with the combined ET-receptor blocker, bosentan (0.5 mg/kg plus 1 mg [center dot] kg [center dot] h, group V, n = 5). The ETB-receptor agonist sarafotoxin 6c (5 ng [center dot] kg [center dot] min; n = 4) was also infused. The percentage change in coronary artery diameter (%Delta CAD) to the infusions was measured at baseline and after 10 weeks of high-cholesterol diet in all animals. Sarafotoxin 6c mildly reduced %Delta CAD at baseline and 10 weeks (-10 +/- 2% and -12 +/- 3%, respectively). FR-139317 did not attenuate the epicardial vasoconstrictor response to ET-1 at baseline (%Delta CAD -18 +/- 8% for group I versus -12 +/- 6% for group II; P = NS) but did at 10 weeks (%Delta CAD) -77 +/- 14% for group I versus -14 +/- 6% for group II; P < .05). FR-139317 did not affect the response to acetylcholine at baseline (%Delta CAD 5 +/- 2% for group III versus 7 +/- 3% for group IV, P = NS) or at 10 weeks (%Delta CAD -23 +/- 12% for group III versus -19 +/- 7% for group IV; P = NS). Bosentan did not affect the response to acetylcholine at baseline or 10 weeks. Short-term ET-receptor inhibition in experimental hypercholesterolemia attenuated the enhanced coronary epicardial vasoconstrictor effects of ET-1 but not acetylcholine-induced coronary epicardial vasoconstriction, suggesting that acetylcholine-induced coronary epicardial vasoconstriction may not be mediated by ET receptors. (Arterioscler Thromb Vasc Biol. 1998;18:108-113.)</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.18.1.108</identifier><identifier>PMID: 9445263</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Acetylcholine - pharmacology ; Animals ; Antihypertensive Agents - pharmacology ; Azepines - pharmacology ; Biological and medical sciences ; Blood Pressure - drug effects ; Bosentan ; Cholesterol - blood ; Coronary Vessels - drug effects ; Coronary Vessels - physiology ; Diet, Atherogenic ; Disorders of blood lipids. Hyperlipoproteinemia ; Endothelin Receptor Antagonists ; Endothelin-1 - pharmacology ; Hemodynamics - drug effects ; Hypercholesterolemia - chemically induced ; Hypercholesterolemia - physiopathology ; Indoles - pharmacology ; Medical sciences ; Metabolic diseases ; Receptors, Endothelin - physiology ; Sulfonamides - pharmacology ; Swine ; Vasoconstriction - drug effects ; Vasoconstriction - physiology ; Vasoconstrictor Agents - pharmacology ; Viper Venoms - pharmacology</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 1998-01, Vol.18 (1), p.108-113</ispartof><rights>1998 American Heart Association, Inc.</rights><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jan 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4676-84a11afebbee3f63420294db3bd7e0192345c31bd1d408de6eff322152c585173</citedby><cites>FETCH-LOGICAL-c4676-84a11afebbee3f63420294db3bd7e0192345c31bd1d408de6eff322152c585173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27902,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2122207$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9445263$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hasdai, David</creatorcontrib><creatorcontrib>Best, Patricia J.M</creatorcontrib><creatorcontrib>Cannan, Charles R</creatorcontrib><creatorcontrib>Mathew, Verghese</creatorcontrib><creatorcontrib>Schwartz, Robert S</creatorcontrib><creatorcontrib>Holmes, David R. Jr</creatorcontrib><creatorcontrib>Lerman, Amir</creatorcontrib><title>Acute Endothelin-Receptor Inhibition Does Not Attenuate Acetylcholine-Induced Coronary Vasoconstriction in Experimental Hypercholesterolemia</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>Endothelin (ET) may mediate the enhanced coronary vasoconstriction associated with hypercholesterolemia. We hypothesized that short-term inhibition of ET receptors attenuates the coronary epicardial vasoconstrictor response to acetylcholine in experimental hypercholesterolemia. ET-1 (group I, n = 5; 5 ng [center dot] kg [center dot] min) and acetylcholine (group III, n = 7; 10 to 10 mol/L) were given by intracoronary infusion in pigs. ET-1 and acetylcholine were also infused with the specific ETA-receptor blocker FR-139317 (5 micro gram [center dot] kg [center dot] min (); group II, n = 6; group IV, n = 6). Acetylcholine was also infused with the combined ET-receptor blocker, bosentan (0.5 mg/kg plus 1 mg [center dot] kg [center dot] h, group V, n = 5). The ETB-receptor agonist sarafotoxin 6c (5 ng [center dot] kg [center dot] min; n = 4) was also infused. The percentage change in coronary artery diameter (%Delta CAD) to the infusions was measured at baseline and after 10 weeks of high-cholesterol diet in all animals. Sarafotoxin 6c mildly reduced %Delta CAD at baseline and 10 weeks (-10 +/- 2% and -12 +/- 3%, respectively). FR-139317 did not attenuate the epicardial vasoconstrictor response to ET-1 at baseline (%Delta CAD -18 +/- 8% for group I versus -12 +/- 6% for group II; P = NS) but did at 10 weeks (%Delta CAD) -77 +/- 14% for group I versus -14 +/- 6% for group II; P < .05). FR-139317 did not affect the response to acetylcholine at baseline (%Delta CAD 5 +/- 2% for group III versus 7 +/- 3% for group IV, P = NS) or at 10 weeks (%Delta CAD -23 +/- 12% for group III versus -19 +/- 7% for group IV; P = NS). Bosentan did not affect the response to acetylcholine at baseline or 10 weeks. Short-term ET-receptor inhibition in experimental hypercholesterolemia attenuated the enhanced coronary epicardial vasoconstrictor effects of ET-1 but not acetylcholine-induced coronary epicardial vasoconstriction, suggesting that acetylcholine-induced coronary epicardial vasoconstriction may not be mediated by ET receptors. (Arterioscler Thromb Vasc Biol. 1998;18:108-113.)</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Azepines - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Bosentan</subject><subject>Cholesterol - blood</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - physiology</subject><subject>Diet, Atherogenic</subject><subject>Disorders of blood lipids. Hyperlipoproteinemia</subject><subject>Endothelin Receptor Antagonists</subject><subject>Endothelin-1 - pharmacology</subject><subject>Hemodynamics - drug effects</subject><subject>Hypercholesterolemia - chemically induced</subject><subject>Hypercholesterolemia - physiopathology</subject><subject>Indoles - pharmacology</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Receptors, Endothelin - physiology</subject><subject>Sulfonamides - pharmacology</subject><subject>Swine</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstriction - physiology</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Viper Venoms - pharmacology</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9UcFu1DAQjRColMKZE1KEuCb12I43OUbL0q5UgYRKr5bjTJSUrL3Yjsr-Ax_dWXbVgzUez3tvxm-y7COwEkDBNYOyvX8ooS6hBFa_yi6h4rKQSqjXdGerpqiU5G-zdzE-MsYk5-wiu2ikrLgSl9m_1i4J843rfRpxnlzxEy3ukw_51o1TN6XJu_yrx5h_9ylvU0K3GGK0FtNhtqMnDhZb1y8W-3ztg3cmHPIHE731LqYw2f8Sk8s3f_cYph26ZOb89kDJkY4xYaCwm8z77M1g5ogfzvEq-_Vtc7--Le5-3GzX7V1hpVqpopYGwAzYdYhiUEJyxhvZd6LrV8ig4UJWVkDXQy9Z3aPCYRCckzG2qitYiavs80l3H_yfhQbQj34JjlpqTg41qpZAoOsTyAYfY8BB72l4-psGpo_eawaavNdQa6C3mhifzrJLt8P-BX82m-pfznUTrZmHYJyd4guMA6flHKeTJ9iTn8ma-HtenjDoEc2cRn3coVCsKqBpagaUFnRAiWc3BJ5t</recordid><startdate>199801</startdate><enddate>199801</enddate><creator>Hasdai, David</creator><creator>Best, Patricia J.M</creator><creator>Cannan, Charles R</creator><creator>Mathew, Verghese</creator><creator>Schwartz, Robert S</creator><creator>Holmes, David R. Jr</creator><creator>Lerman, Amir</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></search><sort><creationdate>199801</creationdate><title>Acute Endothelin-Receptor Inhibition Does Not Attenuate Acetylcholine-Induced Coronary Vasoconstriction in Experimental Hypercholesterolemia</title><author>Hasdai, David ; Best, Patricia J.M ; Cannan, Charles R ; Mathew, Verghese ; Schwartz, Robert S ; Holmes, David R. 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Hyperlipoproteinemia</topic><topic>Endothelin Receptor Antagonists</topic><topic>Endothelin-1 - pharmacology</topic><topic>Hemodynamics - drug effects</topic><topic>Hypercholesterolemia - chemically induced</topic><topic>Hypercholesterolemia - physiopathology</topic><topic>Indoles - pharmacology</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Receptors, Endothelin - physiology</topic><topic>Sulfonamides - pharmacology</topic><topic>Swine</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstriction - physiology</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Viper Venoms - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hasdai, David</creatorcontrib><creatorcontrib>Best, Patricia J.M</creatorcontrib><creatorcontrib>Cannan, Charles R</creatorcontrib><creatorcontrib>Mathew, Verghese</creatorcontrib><creatorcontrib>Schwartz, Robert S</creatorcontrib><creatorcontrib>Holmes, David R. Jr</creatorcontrib><creatorcontrib>Lerman, Amir</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><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hasdai, David</au><au>Best, Patricia J.M</au><au>Cannan, Charles R</au><au>Mathew, Verghese</au><au>Schwartz, Robert S</au><au>Holmes, David R. Jr</au><au>Lerman, Amir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute Endothelin-Receptor Inhibition Does Not Attenuate Acetylcholine-Induced Coronary Vasoconstriction in Experimental Hypercholesterolemia</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>1998-01</date><risdate>1998</risdate><volume>18</volume><issue>1</issue><spage>108</spage><epage>113</epage><pages>108-113</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>Endothelin (ET) may mediate the enhanced coronary vasoconstriction associated with hypercholesterolemia. We hypothesized that short-term inhibition of ET receptors attenuates the coronary epicardial vasoconstrictor response to acetylcholine in experimental hypercholesterolemia. ET-1 (group I, n = 5; 5 ng [center dot] kg [center dot] min) and acetylcholine (group III, n = 7; 10 to 10 mol/L) were given by intracoronary infusion in pigs. ET-1 and acetylcholine were also infused with the specific ETA-receptor blocker FR-139317 (5 micro gram [center dot] kg [center dot] min (); group II, n = 6; group IV, n = 6). Acetylcholine was also infused with the combined ET-receptor blocker, bosentan (0.5 mg/kg plus 1 mg [center dot] kg [center dot] h, group V, n = 5). The ETB-receptor agonist sarafotoxin 6c (5 ng [center dot] kg [center dot] min; n = 4) was also infused. The percentage change in coronary artery diameter (%Delta CAD) to the infusions was measured at baseline and after 10 weeks of high-cholesterol diet in all animals. Sarafotoxin 6c mildly reduced %Delta CAD at baseline and 10 weeks (-10 +/- 2% and -12 +/- 3%, respectively). FR-139317 did not attenuate the epicardial vasoconstrictor response to ET-1 at baseline (%Delta CAD -18 +/- 8% for group I versus -12 +/- 6% for group II; P = NS) but did at 10 weeks (%Delta CAD) -77 +/- 14% for group I versus -14 +/- 6% for group II; P < .05). FR-139317 did not affect the response to acetylcholine at baseline (%Delta CAD 5 +/- 2% for group III versus 7 +/- 3% for group IV, P = NS) or at 10 weeks (%Delta CAD -23 +/- 12% for group III versus -19 +/- 7% for group IV; P = NS). Bosentan did not affect the response to acetylcholine at baseline or 10 weeks. Short-term ET-receptor inhibition in experimental hypercholesterolemia attenuated the enhanced coronary epicardial vasoconstrictor effects of ET-1 but not acetylcholine-induced coronary epicardial vasoconstriction, suggesting that acetylcholine-induced coronary epicardial vasoconstriction may not be mediated by ET receptors. (Arterioscler Thromb Vasc Biol. 1998;18:108-113.)</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>9445263</pmid><doi>10.1161/01.ATV.18.1.108</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 1998-01, Vol.18 (1), p.108-113 |
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| source | Journals@Ovid Ovid Autoload; MEDLINE; Alma/SFX Local Collection |
| subjects | Acetylcholine - pharmacology Animals Antihypertensive Agents - pharmacology Azepines - pharmacology Biological and medical sciences Blood Pressure - drug effects Bosentan Cholesterol - blood Coronary Vessels - drug effects Coronary Vessels - physiology Diet, Atherogenic Disorders of blood lipids. Hyperlipoproteinemia Endothelin Receptor Antagonists Endothelin-1 - pharmacology Hemodynamics - drug effects Hypercholesterolemia - chemically induced Hypercholesterolemia - physiopathology Indoles - pharmacology Medical sciences Metabolic diseases Receptors, Endothelin - physiology Sulfonamides - pharmacology Swine Vasoconstriction - drug effects Vasoconstriction - physiology Vasoconstrictor Agents - pharmacology Viper Venoms - pharmacology |
| title | Acute Endothelin-Receptor Inhibition Does Not Attenuate Acetylcholine-Induced Coronary Vasoconstriction in Experimental Hypercholesterolemia |
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