Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat
1. We have examined the effect of bradykinin on impulse traffic in sympathetic afferent fibres from the heart, great vessels and pleura, and have attempted to identify cardiac nociceptors that on the basis of their functional characteristics might have a role in the initiation of cardiac pain. 2. In...
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description | 1. We have examined the effect of bradykinin on impulse traffic in sympathetic afferent fibres from the heart, great vessels
and pleura, and have attempted to identify cardiac nociceptors that on the basis of their functional characteristics might
have a role in the initiation of cardiac pain. 2. In anaesthetized cats, we recorded afferent impulses from 'single-fibre'
slips of the left 2nd--5th thoracic rami communicantes and associated chain, and selected fibres arising from endings in the
heart, great vessels, pericardium and pleura. We applied bradykinin solution (0 . 1--1 . 0 microgram/ml.) locally to the site
of the ending; we also injected bradykinin (0 . 3--1 . 0 microgram/kg) into the left atrium. 3. Afferent endings excited by
bradykinin (159 of 191 tested) were of two types. The larger group (140) were primarily mechanoreceptors with A delta of C
fibres (mean conduction velocity, 7 . 5 +/- 0 . 6 m/sec). They were very sensitive to light touch. Those located in the heart,
great vessels or overlying pleura had a cardiac rhythm of discharge and were stimulated by an increase in blood pressure or
cardiac volume. 4. Bradykinin increased mechanoreceptor firing from 0 . 7 +/- to 5 . 0 +/- 0 . 3 (mean +/- S.E. of mean) impulses/sec.
Some endings appeared to be stimulated directly by bradykinin, others sensitized by it so that they responded more vigorously
to the pulsatile mechanical stimulation associated with the cardiac cycle. 5. The smaller group of eighteen endings, of which
ten were in the left ventricle, were primarily chemosensitive. Most had C fibres, a few had A delta fibres (mean conduction
velocity, 2 . 3 +/- 0 . 7 m/sec). They were insensitive to light touch. With one exception they never fired with a cardiac
rhythm, and even large increases in aortic or left ventricular pressure had little effect on impulse frequency. 6. Chemosensitive
endings were stimulated by bradykinin, impulse activity increasing from 0 . 6 to 15 . 6 +/- 1 . 3 impulses/sec and remaining
above the control level for 1-3 min. The evoked discharge, which was either continuous or occurred in irregular bursts, was
not secondary to mechanical changes in the heart and great vessels. 7. Tachyphylaxis occurred when the interval between successive
applications of bradykinin was 20 min or less. It was a feature of the response of both mechanosensitive and chemosensitive
endings. 8. Because of their responsiveness to changes in pressure and their sensitivity to light touch, the mec |
doi_str_mv | 10.1113/jphysiol.1980.sp013412 |
format | Article |
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and pleura, and have attempted to identify cardiac nociceptors that on the basis of their functional characteristics might
have a role in the initiation of cardiac pain. 2. In anaesthetized cats, we recorded afferent impulses from 'single-fibre'
slips of the left 2nd--5th thoracic rami communicantes and associated chain, and selected fibres arising from endings in the
heart, great vessels, pericardium and pleura. We applied bradykinin solution (0 . 1--1 . 0 microgram/ml.) locally to the site
of the ending; we also injected bradykinin (0 . 3--1 . 0 microgram/kg) into the left atrium. 3. Afferent endings excited by
bradykinin (159 of 191 tested) were of two types. The larger group (140) were primarily mechanoreceptors with A delta of C
fibres (mean conduction velocity, 7 . 5 +/- 0 . 6 m/sec). They were very sensitive to light touch. Those located in the heart,
great vessels or overlying pleura had a cardiac rhythm of discharge and were stimulated by an increase in blood pressure or
cardiac volume. 4. Bradykinin increased mechanoreceptor firing from 0 . 7 +/- to 5 . 0 +/- 0 . 3 (mean +/- S.E. of mean) impulses/sec.
Some endings appeared to be stimulated directly by bradykinin, others sensitized by it so that they responded more vigorously
to the pulsatile mechanical stimulation associated with the cardiac cycle. 5. The smaller group of eighteen endings, of which
ten were in the left ventricle, were primarily chemosensitive. Most had C fibres, a few had A delta fibres (mean conduction
velocity, 2 . 3 +/- 0 . 7 m/sec). They were insensitive to light touch. With one exception they never fired with a cardiac
rhythm, and even large increases in aortic or left ventricular pressure had little effect on impulse frequency. 6. Chemosensitive
endings were stimulated by bradykinin, impulse activity increasing from 0 . 6 to 15 . 6 +/- 1 . 3 impulses/sec and remaining
above the control level for 1-3 min. The evoked discharge, which was either continuous or occurred in irregular bursts, was
not secondary to mechanical changes in the heart and great vessels. 7. Tachyphylaxis occurred when the interval between successive
applications of bradykinin was 20 min or less. It was a feature of the response of both mechanosensitive and chemosensitive
endings. 8. Because of their responsiveness to changes in pressure and their sensitivity to light touch, the mechanosensitive
endings appear to be unlikely to subserve a primarily nociceptive function, although they may be responsible for evoking some
of the components of the pseudoaffective response. By contrast, the chemosensitive endings appear well fitted to act as cardiac
nociceptors.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.1980.sp013412</identifier><identifier>PMID: 7463375</identifier><language>eng</language><publisher>England: The Physiological Society</publisher><subject>Action Potentials - drug effects ; Animals ; Bradykinin - pharmacology ; Cats ; Chemoreceptor Cells - drug effects ; Heart - innervation ; Mechanoreceptors - drug effects ; Nerve Fibers - physiology ; Neurons, Afferent - drug effects ; Neurons, Afferent - physiology ; Nociceptors - physiology ; Space life sciences ; Sympathetic Nervous System - drug effects ; Tachyphylaxis</subject><ispartof>The Journal of physiology, 1980-09, Vol.306 (1), p.519-536</ispartof><rights>1980 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5999-aa3599b561034d31f23bbad30f4cb6f7858a38555eb6bc973d15421fdc6d64ec3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1283021/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1283021/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,1412,27905,27906,45555,45556,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7463375$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Baker, D G</creatorcontrib><creatorcontrib>Coleridge, H M</creatorcontrib><creatorcontrib>Coleridge, J C</creatorcontrib><creatorcontrib>Nerdrum, T</creatorcontrib><title>Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>1. We have examined the effect of bradykinin on impulse traffic in sympathetic afferent fibres from the heart, great vessels
and pleura, and have attempted to identify cardiac nociceptors that on the basis of their functional characteristics might
have a role in the initiation of cardiac pain. 2. In anaesthetized cats, we recorded afferent impulses from 'single-fibre'
slips of the left 2nd--5th thoracic rami communicantes and associated chain, and selected fibres arising from endings in the
heart, great vessels, pericardium and pleura. We applied bradykinin solution (0 . 1--1 . 0 microgram/ml.) locally to the site
of the ending; we also injected bradykinin (0 . 3--1 . 0 microgram/kg) into the left atrium. 3. Afferent endings excited by
bradykinin (159 of 191 tested) were of two types. The larger group (140) were primarily mechanoreceptors with A delta of C
fibres (mean conduction velocity, 7 . 5 +/- 0 . 6 m/sec). They were very sensitive to light touch. Those located in the heart,
great vessels or overlying pleura had a cardiac rhythm of discharge and were stimulated by an increase in blood pressure or
cardiac volume. 4. Bradykinin increased mechanoreceptor firing from 0 . 7 +/- to 5 . 0 +/- 0 . 3 (mean +/- S.E. of mean) impulses/sec.
Some endings appeared to be stimulated directly by bradykinin, others sensitized by it so that they responded more vigorously
to the pulsatile mechanical stimulation associated with the cardiac cycle. 5. The smaller group of eighteen endings, of which
ten were in the left ventricle, were primarily chemosensitive. Most had C fibres, a few had A delta fibres (mean conduction
velocity, 2 . 3 +/- 0 . 7 m/sec). They were insensitive to light touch. With one exception they never fired with a cardiac
rhythm, and even large increases in aortic or left ventricular pressure had little effect on impulse frequency. 6. Chemosensitive
endings were stimulated by bradykinin, impulse activity increasing from 0 . 6 to 15 . 6 +/- 1 . 3 impulses/sec and remaining
above the control level for 1-3 min. The evoked discharge, which was either continuous or occurred in irregular bursts, was
not secondary to mechanical changes in the heart and great vessels. 7. Tachyphylaxis occurred when the interval between successive
applications of bradykinin was 20 min or less. It was a feature of the response of both mechanosensitive and chemosensitive
endings. 8. Because of their responsiveness to changes in pressure and their sensitivity to light touch, the mechanosensitive
endings appear to be unlikely to subserve a primarily nociceptive function, although they may be responsible for evoking some
of the components of the pseudoaffective response. By contrast, the chemosensitive endings appear well fitted to act as cardiac
nociceptors.</description><subject>Action Potentials - drug effects</subject><subject>Animals</subject><subject>Bradykinin - pharmacology</subject><subject>Cats</subject><subject>Chemoreceptor Cells - drug effects</subject><subject>Heart - innervation</subject><subject>Mechanoreceptors - drug effects</subject><subject>Nerve Fibers - physiology</subject><subject>Neurons, Afferent - drug effects</subject><subject>Neurons, Afferent - physiology</subject><subject>Nociceptors - physiology</subject><subject>Space life sciences</subject><subject>Sympathetic Nervous System - drug effects</subject><subject>Tachyphylaxis</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1980</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkktv1DAUhS0EKkPhJ4C8AjYZ7PiRmAUSVDxVCSTK2nIce-KSsVPb05J_j6NMK9ggVle-9zvH1zoG4BlGW4wxeXU5DXNyYdxi0aJtmhAmFNf3wAZTLqqmEeQ-2CBU1xVpGH4IHqV0iQqEhDgBJw3lpPQ34Nd3o6IeoA0RKqhV7J3S0AfttJlyiK9hym5_GFV2wcNuhl1U_fzTeedhsDDN-0nlwWSnobLWROMz9CZeG2h87_wuwQIWAA7lnrxIloNW-TF4YNWYzJNjPQU_Pry_OPtUnX_9-Pns7XmlmRCiUoqU2jGOEaE9wbYmXad6gizVHbdNy1pFWsaY6XinRUN6zGiNba95z6nR5BS8WX2nQ7c3vS4LRjXKKbq9irMMysm_J94NcheuJa5bgmpcDJ4fDWK4OpiU5d4lbcZReRMOSTaM0rIbKuDLf4KYCypKLqwtKF9RHUNK0di7fTCSS7zyNl65xCtv4y3Cp3--5k52zLPM363zGzea-T9d5cWXb0uDII4ZFsXkxWoyuN1w46KRqyyVX2HyLAsnsVzI3yDnyXk</recordid><startdate>19800901</startdate><enddate>19800901</enddate><creator>Baker, D G</creator><creator>Coleridge, H M</creator><creator>Coleridge, J C</creator><creator>Nerdrum, T</creator><general>The Physiological Society</general><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>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19800901</creationdate><title>Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat</title><author>Baker, D G ; Coleridge, H M ; Coleridge, J C ; Nerdrum, T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5999-aa3599b561034d31f23bbad30f4cb6f7858a38555eb6bc973d15421fdc6d64ec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1980</creationdate><topic>Action Potentials - drug effects</topic><topic>Animals</topic><topic>Bradykinin - pharmacology</topic><topic>Cats</topic><topic>Chemoreceptor Cells - drug effects</topic><topic>Heart - innervation</topic><topic>Mechanoreceptors - drug effects</topic><topic>Nerve Fibers - physiology</topic><topic>Neurons, Afferent - drug effects</topic><topic>Neurons, Afferent - physiology</topic><topic>Nociceptors - physiology</topic><topic>Space life sciences</topic><topic>Sympathetic Nervous System - drug effects</topic><topic>Tachyphylaxis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Baker, D G</creatorcontrib><creatorcontrib>Coleridge, H M</creatorcontrib><creatorcontrib>Coleridge, J C</creatorcontrib><creatorcontrib>Nerdrum, T</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baker, D G</au><au>Coleridge, H M</au><au>Coleridge, J C</au><au>Nerdrum, T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1980-09-01</date><risdate>1980</risdate><volume>306</volume><issue>1</issue><spage>519</spage><epage>536</epage><pages>519-536</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>1. We have examined the effect of bradykinin on impulse traffic in sympathetic afferent fibres from the heart, great vessels
and pleura, and have attempted to identify cardiac nociceptors that on the basis of their functional characteristics might
have a role in the initiation of cardiac pain. 2. In anaesthetized cats, we recorded afferent impulses from 'single-fibre'
slips of the left 2nd--5th thoracic rami communicantes and associated chain, and selected fibres arising from endings in the
heart, great vessels, pericardium and pleura. We applied bradykinin solution (0 . 1--1 . 0 microgram/ml.) locally to the site
of the ending; we also injected bradykinin (0 . 3--1 . 0 microgram/kg) into the left atrium. 3. Afferent endings excited by
bradykinin (159 of 191 tested) were of two types. The larger group (140) were primarily mechanoreceptors with A delta of C
fibres (mean conduction velocity, 7 . 5 +/- 0 . 6 m/sec). They were very sensitive to light touch. Those located in the heart,
great vessels or overlying pleura had a cardiac rhythm of discharge and were stimulated by an increase in blood pressure or
cardiac volume. 4. Bradykinin increased mechanoreceptor firing from 0 . 7 +/- to 5 . 0 +/- 0 . 3 (mean +/- S.E. of mean) impulses/sec.
Some endings appeared to be stimulated directly by bradykinin, others sensitized by it so that they responded more vigorously
to the pulsatile mechanical stimulation associated with the cardiac cycle. 5. The smaller group of eighteen endings, of which
ten were in the left ventricle, were primarily chemosensitive. Most had C fibres, a few had A delta fibres (mean conduction
velocity, 2 . 3 +/- 0 . 7 m/sec). They were insensitive to light touch. With one exception they never fired with a cardiac
rhythm, and even large increases in aortic or left ventricular pressure had little effect on impulse frequency. 6. Chemosensitive
endings were stimulated by bradykinin, impulse activity increasing from 0 . 6 to 15 . 6 +/- 1 . 3 impulses/sec and remaining
above the control level for 1-3 min. The evoked discharge, which was either continuous or occurred in irregular bursts, was
not secondary to mechanical changes in the heart and great vessels. 7. Tachyphylaxis occurred when the interval between successive
applications of bradykinin was 20 min or less. It was a feature of the response of both mechanosensitive and chemosensitive
endings. 8. Because of their responsiveness to changes in pressure and their sensitivity to light touch, the mechanosensitive
endings appear to be unlikely to subserve a primarily nociceptive function, although they may be responsible for evoking some
of the components of the pseudoaffective response. By contrast, the chemosensitive endings appear well fitted to act as cardiac
nociceptors.</abstract><cop>England</cop><pub>The Physiological Society</pub><pmid>7463375</pmid><doi>10.1113/jphysiol.1980.sp013412</doi><tpages>18</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; Wiley Online Library Journals Frontfile Complete; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
subjects | Action Potentials - drug effects Animals Bradykinin - pharmacology Cats Chemoreceptor Cells - drug effects Heart - innervation Mechanoreceptors - drug effects Nerve Fibers - physiology Neurons, Afferent - drug effects Neurons, Afferent - physiology Nociceptors - physiology Space life sciences Sympathetic Nervous System - drug effects Tachyphylaxis |
title | Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat |
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