Cardiovascular agents affect the tone of pulmonary arteries and veins in precision-cut lung slices
Cardiovascular agents are pivotal in the therapy of heart failure. Apart from their action on ventricular contractility and systemic afterload, they affect pulmonary arteries and veins. Although these effects are crucial in heart failure with coexisting pulmonary hypertension or lung oedema, they ar...
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| description | Cardiovascular agents are pivotal in the therapy of heart failure. Apart from their action on ventricular contractility and systemic afterload, they affect pulmonary arteries and veins. Although these effects are crucial in heart failure with coexisting pulmonary hypertension or lung oedema, they are poorly defined, especially in pulmonary veins. Therefore, we investigated the pulmonary vascular effects of adrenoceptor agonists, vasopressin and angiotensin II in the model of precision-cut lung slices that allows simultaneous studies of pulmonary arteries and veins.
Precision-cut lung slices were prepared from guinea pigs and imaged by videomicroscopy. Concentration-response curves of cardiovascular drugs were analysed in pulmonary arteries and veins.
Pulmonary veins responded stronger than arteries to α(1)-agonists (contraction) and β(2)-agonists (relaxation). Notably, inhibition of β(2)-adrenoceptors unmasked the α(1)-mimetic effect of norepinephrine and epinephrine in pulmonary veins. Vasopressin and angiotensin II contracted pulmonary veins via V(1a) and AT(1) receptors, respectively, without affecting pulmonary arteries.
Vasopressin and (nor)epinephrine in combination with β(2)-inhibition caused pulmonary venoconstriction. If applicable in humans, these treatments would enhance capillary hydrostatic pressures and lung oedema, suggesting their cautious use in left heart failure. Vice versa, the prevention of pulmonary venoconstriction by AT(1) receptor antagonists might contribute to their beneficial effects seen in left heart failure. Further, α(1)-mimetic agents might exacerbate pulmonary hypertension and right ventricular failure by contracting pulmonary arteries, whereas vasopressin might not. |
| doi_str_mv | 10.1371/journal.pone.0029698 |
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Precision-cut lung slices were prepared from guinea pigs and imaged by videomicroscopy. Concentration-response curves of cardiovascular drugs were analysed in pulmonary arteries and veins.
Pulmonary veins responded stronger than arteries to α(1)-agonists (contraction) and β(2)-agonists (relaxation). Notably, inhibition of β(2)-adrenoceptors unmasked the α(1)-mimetic effect of norepinephrine and epinephrine in pulmonary veins. Vasopressin and angiotensin II contracted pulmonary veins via V(1a) and AT(1) receptors, respectively, without affecting pulmonary arteries.
Vasopressin and (nor)epinephrine in combination with β(2)-inhibition caused pulmonary venoconstriction. If applicable in humans, these treatments would enhance capillary hydrostatic pressures and lung oedema, suggesting their cautious use in left heart failure. Vice versa, the prevention of pulmonary venoconstriction by AT(1) receptor antagonists might contribute to their beneficial effects seen in left heart failure. Further, α(1)-mimetic agents might exacerbate pulmonary hypertension and right ventricular failure by contracting pulmonary arteries, whereas vasopressin might not.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0029698</identifier><identifier>PMID: 22216346</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adrenergic receptors ; Anesthesiology ; Angiotensin ; Angiotensin II ; Angiotensins ; Animals ; Argipressin receptors ; Arteries ; Capillary pressure ; Cardiovascular agents ; Cardiovascular Agents - pharmacology ; Contraction ; Coronary vessels ; Dose-Response Relationship, Drug ; Drugs ; Edema ; Endothelium ; Enzymes ; Epinephrine ; Female ; Guinea Pigs ; Heart ; Heart diseases ; Heart failure ; Heart surgery ; Histology ; Hypertension ; In Vitro Techniques ; Inhibition ; Localization ; Lung - blood supply ; Lungs ; Medicine ; Muscle contraction ; Muscle Tonus - drug effects ; Norepinephrine ; Pharmacology ; Pulmonary arteries ; Pulmonary artery ; Pulmonary Artery - drug effects ; Pulmonary Artery - physiology ; Pulmonary hypertension ; Pulmonary Veins - drug effects ; Pulmonary Veins - physiology ; Receptors ; Receptors (physiology) ; Right ventricular failure ; Rodents ; Studies ; Toxicology ; Vasopressin ; Veins ; Veins & arteries ; Ventricle</subject><ispartof>PloS one, 2011-12, Vol.6 (12), p.e29698</ispartof><rights>2011 Rieg et al.</rights><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Rieg et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Rieg et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c757t-db971c05c1c308e253e05653baf13b74dabd02ab8270ab5d25ce95572c3cab913</citedby><cites>FETCH-LOGICAL-c757t-db971c05c1c308e253e05653baf13b74dabd02ab8270ab5d25ce95572c3cab913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246495/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246495/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22216346$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kolb, Martin R. J.</contributor><creatorcontrib>Rieg, Annette D</creatorcontrib><creatorcontrib>Rossaint, Rolf</creatorcontrib><creatorcontrib>Uhlig, Stefan</creatorcontrib><creatorcontrib>Martin, Christian</creatorcontrib><title>Cardiovascular agents affect the tone of pulmonary arteries and veins in precision-cut lung slices</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cardiovascular agents are pivotal in the therapy of heart failure. Apart from their action on ventricular contractility and systemic afterload, they affect pulmonary arteries and veins. Although these effects are crucial in heart failure with coexisting pulmonary hypertension or lung oedema, they are poorly defined, especially in pulmonary veins. Therefore, we investigated the pulmonary vascular effects of adrenoceptor agonists, vasopressin and angiotensin II in the model of precision-cut lung slices that allows simultaneous studies of pulmonary arteries and veins.
Precision-cut lung slices were prepared from guinea pigs and imaged by videomicroscopy. Concentration-response curves of cardiovascular drugs were analysed in pulmonary arteries and veins.
Pulmonary veins responded stronger than arteries to α(1)-agonists (contraction) and β(2)-agonists (relaxation). Notably, inhibition of β(2)-adrenoceptors unmasked the α(1)-mimetic effect of norepinephrine and epinephrine in pulmonary veins. Vasopressin and angiotensin II contracted pulmonary veins via V(1a) and AT(1) receptors, respectively, without affecting pulmonary arteries.
Vasopressin and (nor)epinephrine in combination with β(2)-inhibition caused pulmonary venoconstriction. If applicable in humans, these treatments would enhance capillary hydrostatic pressures and lung oedema, suggesting their cautious use in left heart failure. Vice versa, the prevention of pulmonary venoconstriction by AT(1) receptor antagonists might contribute to their beneficial effects seen in left heart failure. Further, α(1)-mimetic agents might exacerbate pulmonary hypertension and right ventricular failure by contracting pulmonary arteries, whereas vasopressin might not.</description><subject>Adrenergic receptors</subject><subject>Anesthesiology</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensins</subject><subject>Animals</subject><subject>Argipressin receptors</subject><subject>Arteries</subject><subject>Capillary pressure</subject><subject>Cardiovascular agents</subject><subject>Cardiovascular Agents - pharmacology</subject><subject>Contraction</subject><subject>Coronary vessels</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drugs</subject><subject>Edema</subject><subject>Endothelium</subject><subject>Enzymes</subject><subject>Epinephrine</subject><subject>Female</subject><subject>Guinea Pigs</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart surgery</subject><subject>Histology</subject><subject>Hypertension</subject><subject>In Vitro Techniques</subject><subject>Inhibition</subject><subject>Localization</subject><subject>Lung - blood supply</subject><subject>Lungs</subject><subject>Medicine</subject><subject>Muscle contraction</subject><subject>Muscle Tonus - drug effects</subject><subject>Norepinephrine</subject><subject>Pharmacology</subject><subject>Pulmonary arteries</subject><subject>Pulmonary artery</subject><subject>Pulmonary Artery - drug effects</subject><subject>Pulmonary Artery - physiology</subject><subject>Pulmonary hypertension</subject><subject>Pulmonary Veins - drug effects</subject><subject>Pulmonary Veins - physiology</subject><subject>Receptors</subject><subject>Receptors (physiology)</subject><subject>Right ventricular failure</subject><subject>Rodents</subject><subject>Studies</subject><subject>Toxicology</subject><subject>Vasopressin</subject><subject>Veins</subject><subject>Veins & arteries</subject><subject>Ventricle</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QDguDFjPlo2uZGWAY_BhYW_LoNp-lpJ0OnGZN00H9vxukuU1CQXCQkz3mT8-bNsueMLpko2dutG_0A_XLvBlxSylWhqgfZJVOCLwpOxcOz9UX2JIQtpVJURfE4u-Ccs0LkxWVWr8A31h0gmLEHT6DDIQYCbYsmkrhBEpM-cS3Zj_3ODeB_EfARvcVEDQ05oB0CsQPZezQ2WDcszBhJPw4dCb01GJ5mj1roAz6b5qvs24f3X1efFje3H9er65uFKWUZF02tSmaoNMwIWiGXAqkspKihZaIu8wbqhnKoK15SqGXDpUElZcmNMFArJq6ylyfdfe-CnuwJmglWlUoVBU_E-kQ0DrZ67-0utaMdWP1nw_lOp96s6VHnoqrBcAQKmKuyBQ6GoqpEXjU1KpW03k23jfUOG5Ns89DPROcng93ozh204HmRK5kEXk0C3v0YMcR_PHmiOkivskPrkpjZ2WD0dV4WlayYPLa-_AuVRoM7a9IHtjbtzwrezAoSE_Fn7GAMQa-_fP5_9vb7nH19xm4Q-rgJrh9jykWYg_kJNN6F4LG9d45Rfcz3nRv6mG895TuVvTh3_b7oLtDiNxhh90s</recordid><startdate>20111227</startdate><enddate>20111227</enddate><creator>Rieg, Annette D</creator><creator>Rossaint, Rolf</creator><creator>Uhlig, Stefan</creator><creator>Martin, Christian</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20111227</creationdate><title>Cardiovascular agents affect the tone of pulmonary arteries and veins in precision-cut lung slices</title><author>Rieg, Annette D ; Rossaint, Rolf ; Uhlig, Stefan ; Martin, Christian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c757t-db971c05c1c308e253e05653baf13b74dabd02ab8270ab5d25ce95572c3cab913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adrenergic receptors</topic><topic>Anesthesiology</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensins</topic><topic>Animals</topic><topic>Argipressin receptors</topic><topic>Arteries</topic><topic>Capillary pressure</topic><topic>Cardiovascular agents</topic><topic>Cardiovascular Agents - pharmacology</topic><topic>Contraction</topic><topic>Coronary vessels</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drugs</topic><topic>Edema</topic><topic>Endothelium</topic><topic>Enzymes</topic><topic>Epinephrine</topic><topic>Female</topic><topic>Guinea Pigs</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Heart surgery</topic><topic>Histology</topic><topic>Hypertension</topic><topic>In Vitro Techniques</topic><topic>Inhibition</topic><topic>Localization</topic><topic>Lung - blood supply</topic><topic>Lungs</topic><topic>Medicine</topic><topic>Muscle contraction</topic><topic>Muscle Tonus - drug effects</topic><topic>Norepinephrine</topic><topic>Pharmacology</topic><topic>Pulmonary arteries</topic><topic>Pulmonary artery</topic><topic>Pulmonary Artery - drug effects</topic><topic>Pulmonary Artery - physiology</topic><topic>Pulmonary hypertension</topic><topic>Pulmonary Veins - drug effects</topic><topic>Pulmonary Veins - physiology</topic><topic>Receptors</topic><topic>Receptors (physiology)</topic><topic>Right ventricular failure</topic><topic>Rodents</topic><topic>Studies</topic><topic>Toxicology</topic><topic>Vasopressin</topic><topic>Veins</topic><topic>Veins & arteries</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rieg, Annette D</creatorcontrib><creatorcontrib>Rossaint, Rolf</creatorcontrib><creatorcontrib>Uhlig, Stefan</creatorcontrib><creatorcontrib>Martin, Christian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiovascular agents affect the tone of pulmonary arteries and veins in precision-cut lung slices</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-12-27</date><risdate>2011</risdate><volume>6</volume><issue>12</issue><spage>e29698</spage><pages>e29698-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Cardiovascular agents are pivotal in the therapy of heart failure. Apart from their action on ventricular contractility and systemic afterload, they affect pulmonary arteries and veins. Although these effects are crucial in heart failure with coexisting pulmonary hypertension or lung oedema, they are poorly defined, especially in pulmonary veins. Therefore, we investigated the pulmonary vascular effects of adrenoceptor agonists, vasopressin and angiotensin II in the model of precision-cut lung slices that allows simultaneous studies of pulmonary arteries and veins.
Precision-cut lung slices were prepared from guinea pigs and imaged by videomicroscopy. Concentration-response curves of cardiovascular drugs were analysed in pulmonary arteries and veins.
Pulmonary veins responded stronger than arteries to α(1)-agonists (contraction) and β(2)-agonists (relaxation). Notably, inhibition of β(2)-adrenoceptors unmasked the α(1)-mimetic effect of norepinephrine and epinephrine in pulmonary veins. Vasopressin and angiotensin II contracted pulmonary veins via V(1a) and AT(1) receptors, respectively, without affecting pulmonary arteries.
Vasopressin and (nor)epinephrine in combination with β(2)-inhibition caused pulmonary venoconstriction. If applicable in humans, these treatments would enhance capillary hydrostatic pressures and lung oedema, suggesting their cautious use in left heart failure. Vice versa, the prevention of pulmonary venoconstriction by AT(1) receptor antagonists might contribute to their beneficial effects seen in left heart failure. Further, α(1)-mimetic agents might exacerbate pulmonary hypertension and right ventricular failure by contracting pulmonary arteries, whereas vasopressin might not.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22216346</pmid><doi>10.1371/journal.pone.0029698</doi><tpages>e29698</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adrenergic receptors Anesthesiology Angiotensin Angiotensin II Angiotensins Animals Argipressin receptors Arteries Capillary pressure Cardiovascular agents Cardiovascular Agents - pharmacology Contraction Coronary vessels Dose-Response Relationship, Drug Drugs Edema Endothelium Enzymes Epinephrine Female Guinea Pigs Heart Heart diseases Heart failure Heart surgery Histology Hypertension In Vitro Techniques Inhibition Localization Lung - blood supply Lungs Medicine Muscle contraction Muscle Tonus - drug effects Norepinephrine Pharmacology Pulmonary arteries Pulmonary artery Pulmonary Artery - drug effects Pulmonary Artery - physiology Pulmonary hypertension Pulmonary Veins - drug effects Pulmonary Veins - physiology Receptors Receptors (physiology) Right ventricular failure Rodents Studies Toxicology Vasopressin Veins Veins & arteries Ventricle |
| title | Cardiovascular agents affect the tone of pulmonary arteries and veins in precision-cut lung slices |
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