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Prostaglandins Contribute to Activation of Baroreceptors in Rabbits: Possible Paracrine Influence of Endothelium

The purpose of this study was to test the hypothesis that prostaglandins released from vascular endothelial cells contribute to activation of baroreceptors during increases in arterial pressure. Baroreceptor activity was recorded from the vascularly isolated carotid sinus in rabbits anesthetized wit...

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Published in:Circulation research 1990-12, Vol.67 (6), p.1394-1404
Main Authors: Chen, Hsing I, Chapleau, Mark W, McDowell, Thomas S, Abboud, Francois M
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Chapleau, Mark W
McDowell, Thomas S
Abboud, Francois M
description The purpose of this study was to test the hypothesis that prostaglandins released from vascular endothelial cells contribute to activation of baroreceptors during increases in arterial pressure. Baroreceptor activity was recorded from the vascularly isolated carotid sinus in rabbits anesthetized with chloralose. Baroreceptor activity was measured during ramp or step increases in nonpulsatile carotid sinus pressure over a range of 0–175 mm Hg. Exposure of the isolated carotid sinus to inhibitors of prostaglandin formation (indomethacin [n = 10] or aspirin [n=6]) decreased baroreceptor activity significantly (p
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Baroreceptor activity was recorded from the vascularly isolated carotid sinus in rabbits anesthetized with chloralose. Baroreceptor activity was measured during ramp or step increases in nonpulsatile carotid sinus pressure over a range of 0–175 mm Hg. Exposure of the isolated carotid sinus to inhibitors of prostaglandin formation (indomethacin [n = 10] or aspirin [n=6]) decreased baroreceptor activity significantly (p&lt;0.05). The slope of the pressure-activity relation averaged 0.80±0.07 %/mm Hg (mean±SEM) during control measurements and 0.72±0.06 and 0.63±0.05 %/mm Hg during exposure to 10 and 20 μM indomethacin, respectively. Exposure of the carotid sinus to exogenous prostacyclin (PGI2 [n=11]) increased baroreceptor activity significantly. The slope of the pressure-activity relation averaged 0.89±0.10, 1.09±0.09, and 1.26±0.16 %/mm Hg during control and during exposure to 10 and 20 μM PGI2, respectively. Activity returned to control after removal of PGI2 (0.89±0.12 %/mm Hg). Removal of endothelium with either a balloon catheter (n=4) or a jet of a 95% O2-5% CO2 gas mixture (n=6) decreased the slope of the pressure-activity relation from 0.92±0.09 to 0.56±0.08 %/mm Hg (p&lt;0.05). Exposure of the denuded sinus to exogenous PGI2 (20 μM [n=4]) restored activity (slope=1.09±0.24 %/mmHg). Neither indomethacin (n=5) nor PGI2 (n=5) nor denudation (n=5) significantly altered the pressure-diameter relation of the carotid sinus (sonomicrometers), suggesting that the effects on baroreceptor discharge are not caused by altered stretch of the carotid sinus at a given pressure. The results suggest that prostaglandins (e.g., PGI2) released from endothelium contribute in a paracrine manner to activation of baroreceptors during increases in arterial pressure.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.res.67.6.1394</identifier><identifier>PMID: 2245501</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Aspirin - pharmacology ; Biological and medical sciences ; Blood vessels and receptors ; Carotid Sinus - physiology ; Endothelium, Vascular - physiology ; Epoprostenol - pharmacology ; Fundamental and applied biological sciences. 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Removal of endothelium with either a balloon catheter (n=4) or a jet of a 95% O2-5% CO2 gas mixture (n=6) decreased the slope of the pressure-activity relation from 0.92±0.09 to 0.56±0.08 %/mm Hg (p&lt;0.05). Exposure of the denuded sinus to exogenous PGI2 (20 μM [n=4]) restored activity (slope=1.09±0.24 %/mmHg). Neither indomethacin (n=5) nor PGI2 (n=5) nor denudation (n=5) significantly altered the pressure-diameter relation of the carotid sinus (sonomicrometers), suggesting that the effects on baroreceptor discharge are not caused by altered stretch of the carotid sinus at a given pressure. The results suggest that prostaglandins (e.g., PGI2) released from endothelium contribute in a paracrine manner to activation of baroreceptors during increases in arterial pressure.</description><subject>Animals</subject><subject>Aspirin - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood vessels and receptors</subject><subject>Carotid Sinus - physiology</subject><subject>Endothelium, Vascular - physiology</subject><subject>Epoprostenol - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Indomethacin - pharmacology</subject><subject>Male</subject><subject>Microscopy, Electron, Scanning</subject><subject>Pressoreceptors - drug effects</subject><subject>Pressoreceptors - physiology</subject><subject>Prostaglandins - physiology</subject><subject>Rabbits</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><recordid>eNpFkUGP0zAQhS0EWsrCnQuSL3BL8MSOU3NbqgIrrUS1wNlynAk1uHaxHVb8e1y1goM1sua9p5lvCHkJrAWQ8JZBmzC3cmhlC1yJR2QFfSca0Q_wmKwYY6oZOGdPybOcfzAGgnfqilx1neh7Bity3KWYi_nuTZhcyHQTQ0luXArSEumNLe63KS4GGmf63qSY0OKxxJSpC_TejKMr-R3dxZzd6JHuTDI2uYD0Nsx-wWDx5NyGKZY9erccnpMns_EZX1zqNfn2Yft186m5-_zxdnNz19geBGtATnaWlvfMKttLhlxMvRgnobqZczVYPs1rBVxKuR7nyUiD0FW1moZuYJLza_LmnHtM8deCueiDyxZ9XRTjkvW6sgClTkJ2FtpKIiec9TG5g0l_NDB9gqwZ6PvtFy0HLfUJcrW8umQv4wGnf4YL1dp_fembbI2fkwnW5f-5qu9UnbbqxFn3EH3BlH_65QGT3qPxZa_r8Rhn0DV1zFrqr6kPGP8L8wmVRQ</recordid><startdate>199012</startdate><enddate>199012</enddate><creator>Chen, Hsing I</creator><creator>Chapleau, Mark W</creator><creator>McDowell, Thomas S</creator><creator>Abboud, Francois M</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>199012</creationdate><title>Prostaglandins Contribute to Activation of Baroreceptors in Rabbits: Possible Paracrine Influence of Endothelium</title><author>Chen, Hsing I ; Chapleau, Mark W ; McDowell, Thomas S ; Abboud, Francois M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5140-16dcf6c350c9c560e34d54bd492f3397c3df89136668bfda6ae123509d7270633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Animals</topic><topic>Aspirin - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood vessels and receptors</topic><topic>Carotid Sinus - physiology</topic><topic>Endothelium, Vascular - physiology</topic><topic>Epoprostenol - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Indomethacin - pharmacology</topic><topic>Male</topic><topic>Microscopy, Electron, Scanning</topic><topic>Pressoreceptors - drug effects</topic><topic>Pressoreceptors - physiology</topic><topic>Prostaglandins - physiology</topic><topic>Rabbits</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Hsing I</creatorcontrib><creatorcontrib>Chapleau, Mark W</creatorcontrib><creatorcontrib>McDowell, Thomas S</creatorcontrib><creatorcontrib>Abboud, Francois 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>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Hsing I</au><au>Chapleau, Mark W</au><au>McDowell, Thomas S</au><au>Abboud, Francois M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prostaglandins Contribute to Activation of Baroreceptors in Rabbits: Possible Paracrine Influence of Endothelium</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1990-12</date><risdate>1990</risdate><volume>67</volume><issue>6</issue><spage>1394</spage><epage>1404</epage><pages>1394-1404</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>The purpose of this study was to test the hypothesis that prostaglandins released from vascular endothelial cells contribute to activation of baroreceptors during increases in arterial pressure. Baroreceptor activity was recorded from the vascularly isolated carotid sinus in rabbits anesthetized with chloralose. Baroreceptor activity was measured during ramp or step increases in nonpulsatile carotid sinus pressure over a range of 0–175 mm Hg. Exposure of the isolated carotid sinus to inhibitors of prostaglandin formation (indomethacin [n = 10] or aspirin [n=6]) decreased baroreceptor activity significantly (p&lt;0.05). The slope of the pressure-activity relation averaged 0.80±0.07 %/mm Hg (mean±SEM) during control measurements and 0.72±0.06 and 0.63±0.05 %/mm Hg during exposure to 10 and 20 μM indomethacin, respectively. Exposure of the carotid sinus to exogenous prostacyclin (PGI2 [n=11]) increased baroreceptor activity significantly. The slope of the pressure-activity relation averaged 0.89±0.10, 1.09±0.09, and 1.26±0.16 %/mm Hg during control and during exposure to 10 and 20 μM PGI2, respectively. Activity returned to control after removal of PGI2 (0.89±0.12 %/mm Hg). Removal of endothelium with either a balloon catheter (n=4) or a jet of a 95% O2-5% CO2 gas mixture (n=6) decreased the slope of the pressure-activity relation from 0.92±0.09 to 0.56±0.08 %/mm Hg (p&lt;0.05). Exposure of the denuded sinus to exogenous PGI2 (20 μM [n=4]) restored activity (slope=1.09±0.24 %/mmHg). Neither indomethacin (n=5) nor PGI2 (n=5) nor denudation (n=5) significantly altered the pressure-diameter relation of the carotid sinus (sonomicrometers), suggesting that the effects on baroreceptor discharge are not caused by altered stretch of the carotid sinus at a given pressure. The results suggest that prostaglandins (e.g., PGI2) released from endothelium contribute in a paracrine manner to activation of baroreceptors during increases in arterial pressure.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>2245501</pmid><doi>10.1161/01.res.67.6.1394</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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source Freely Accessible Science Journals - check A-Z of ejournals
subjects Animals
Aspirin - pharmacology
Biological and medical sciences
Blood vessels and receptors
Carotid Sinus - physiology
Endothelium, Vascular - physiology
Epoprostenol - pharmacology
Fundamental and applied biological sciences. Psychology
Indomethacin - pharmacology
Male
Microscopy, Electron, Scanning
Pressoreceptors - drug effects
Pressoreceptors - physiology
Prostaglandins - physiology
Rabbits
Vertebrates: cardiovascular system
title Prostaglandins Contribute to Activation of Baroreceptors in Rabbits: Possible Paracrine Influence of Endothelium
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