Plasma Atrial Natriuretic Factor During Chronic Thoracic Inferior Vena Caval Constriction

The effects of chronic constriction of the thoracic inferior vena cava (TIVCC) on plasma atrial natriuretic factor (pANF) were studied in conscious dogs (n = 5). TIVCC decreased left and right atria] pressure and led to a decrease in pANF concentration from 199 ± 12 to 104 ± 14 pg/ml while plasma re...

Full description

Saved in:
Bibliographic Details
Published in:Circulation research 1988-02, Vol.62 (2), p.279-285
Main Authors: Paganelli, William C, Cant, James R, Pintal, Richard R, A, Imre Kifor, Barger, Clifford, Dzau, Victor J
Format: Article
Language:English
Subjects:
Animals
Arginine Vasopressin - blood
Atrial Natriuretic Factor - blood
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure
Cardiology. Vascular system
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Dogs
Male
Medical sciences
Renin - blood
Sodium - metabolism
Vasoconstriction
Vena Cava, Inferior - physiology
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c4430-a6268b5da9943d394a97a2bc024164ff6b840bc13096f6ea6bda24158985d4b13
cites
container_end_page 285
container_issue 2
container_start_page 279
container_title Circulation research
container_volume 62
creator Paganelli, William C
Cant, James R
Pintal, Richard R
A, Imre Kifor
Barger, Clifford
Dzau, Victor J
description The effects of chronic constriction of the thoracic inferior vena cava (TIVCC) on plasma atrial natriuretic factor (pANF) were studied in conscious dogs (n = 5). TIVCC decreased left and right atria] pressure and led to a decrease in pANF concentration from 199 ± 12 to 104 ± 14 pg/ml while plasma renin and vasopressin concentrations increased. These hormonal changes were associated with a significant fall in sodium excretion to
doi_str_mv 10.1161/01.RES.62.2.279
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_78097152</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>78097152</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4430-a6268b5da9943d394a97a2bc024164ff6b840bc13096f6ea6bda24158985d4b13</originalsourceid><addsrcrecordid>eNo9kc1v1DAQxS0EKkvhzAkpB8Qt2_FH7PhYhRYqVYCgIHGyJo7DBrxxaydU_PdMtatqZI3t95tn6Zmx1xy2nGt-Bnz79eLbVostlbFP2IY3QtWqMfwp2wCArY2U8Jy9KOU3AFdS2BN2IqwWplUb9vNLxLLH6nzJE8bqE1Jfc1gmX12iX1Ku3q95mn9V3S6nmW5vdimjp83VPIY8EfAjzFh1-JfGuzQXMvDLlOaX7NmIsYRXx37Kvl9e3HQf6-vPH6668-vaKyWhRi102zcDWqvkIK1Ca1D0HoTiWo2j7lsFvecSrB51QN0PSFLT2rYZVM_lKXt38L3N6W4NZXH7qfgQI84hrcWZFqyhUAg8O4A-p1JyGN1tnvaY_zkO7iFMB9xRmE4LR2UsTbw5Wq_9PgyP_DE90t8edSwe45hx9lN5xEwjlZAPD6sDdp_iEnL5E9f7kN0uYFx2jv4IJHBRc9u2IOhU0-Ig_wNmV4tB</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>78097152</pqid></control><display><type>article</type><title>Plasma Atrial Natriuretic Factor During Chronic Thoracic Inferior Vena Caval Constriction</title><source>Freely Accessible Science Journals</source><creator>Paganelli, William C ; Cant, James R ; Pintal, Richard R ; A, Imre Kifor ; Barger, Clifford ; Dzau, Victor J</creator><creatorcontrib>Paganelli, William C ; Cant, James R ; Pintal, Richard R ; A, Imre Kifor ; Barger, Clifford ; Dzau, Victor J</creatorcontrib><description>The effects of chronic constriction of the thoracic inferior vena cava (TIVCC) on plasma atrial natriuretic factor (pANF) were studied in conscious dogs (n = 5). TIVCC decreased left and right atria] pressure and led to a decrease in pANF concentration from 199 ± 12 to 104 ± 14 pg/ml while plasma renin and vasopressin concentrations increased. These hormonal changes were associated with a significant fall in sodium excretion to &lt;5 meq/day. pANF remained suppressed during chronic TIVCC as the dogs expanded their extracellular fluid volume and developed ascites. Acute release of TIVCC resulted in abrupt increases in left and right atrial pressure but only a modest rise in pANF from 96 ± 16 to 185 ± 45 pg/ml. The magnitude of the rise in pANF (twofold) contrasted sharply with the eightfold increase in sodium excretion that occurred over the first 24 hours. Our data suggest that decrease in atrial pressure below normal results in a decline in pANF, which, acting in concert with the activated renin-angiotensin system and vasopressin, may contribute to sodium retention. On the other hand, during acute release of TIVCC, which markedly increased atrial pressure and sodium excretion, pANF only returned to control levels. These data suggest that ANF release may be attenuated during chronic reduction in atrial pressure and also raise a question concerning the magnitude of the primary role of ANF in this natriuretic response.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.62.2.279</identifier><identifier>PMID: 2962784</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Arginine Vasopressin - blood ; Atrial Natriuretic Factor - blood ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Cardiology. Vascular system ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Dogs ; Male ; Medical sciences ; Renin - blood ; Sodium - metabolism ; Vasoconstriction ; Vena Cava, Inferior - physiology</subject><ispartof>Circulation research, 1988-02, Vol.62 (2), p.279-285</ispartof><rights>1988 American Heart Association, Inc.</rights><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4430-a6268b5da9943d394a97a2bc024164ff6b840bc13096f6ea6bda24158985d4b13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=7534232$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2962784$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Paganelli, William C</creatorcontrib><creatorcontrib>Cant, James R</creatorcontrib><creatorcontrib>Pintal, Richard R</creatorcontrib><creatorcontrib>A, Imre Kifor</creatorcontrib><creatorcontrib>Barger, Clifford</creatorcontrib><creatorcontrib>Dzau, Victor J</creatorcontrib><title>Plasma Atrial Natriuretic Factor During Chronic Thoracic Inferior Vena Caval Constriction</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>The effects of chronic constriction of the thoracic inferior vena cava (TIVCC) on plasma atrial natriuretic factor (pANF) were studied in conscious dogs (n = 5). TIVCC decreased left and right atria] pressure and led to a decrease in pANF concentration from 199 ± 12 to 104 ± 14 pg/ml while plasma renin and vasopressin concentrations increased. These hormonal changes were associated with a significant fall in sodium excretion to &lt;5 meq/day. pANF remained suppressed during chronic TIVCC as the dogs expanded their extracellular fluid volume and developed ascites. Acute release of TIVCC resulted in abrupt increases in left and right atrial pressure but only a modest rise in pANF from 96 ± 16 to 185 ± 45 pg/ml. The magnitude of the rise in pANF (twofold) contrasted sharply with the eightfold increase in sodium excretion that occurred over the first 24 hours. Our data suggest that decrease in atrial pressure below normal results in a decline in pANF, which, acting in concert with the activated renin-angiotensin system and vasopressin, may contribute to sodium retention. On the other hand, during acute release of TIVCC, which markedly increased atrial pressure and sodium excretion, pANF only returned to control levels. These data suggest that ANF release may be attenuated during chronic reduction in atrial pressure and also raise a question concerning the magnitude of the primary role of ANF in this natriuretic response.</description><subject>Animals</subject><subject>Arginine Vasopressin - blood</subject><subject>Atrial Natriuretic Factor - blood</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure</subject><subject>Cardiology. Vascular system</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Dogs</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Renin - blood</subject><subject>Sodium - metabolism</subject><subject>Vasoconstriction</subject><subject>Vena Cava, Inferior - physiology</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><recordid>eNo9kc1v1DAQxS0EKkvhzAkpB8Qt2_FH7PhYhRYqVYCgIHGyJo7DBrxxaydU_PdMtatqZI3t95tn6Zmx1xy2nGt-Bnz79eLbVostlbFP2IY3QtWqMfwp2wCArY2U8Jy9KOU3AFdS2BN2IqwWplUb9vNLxLLH6nzJE8bqE1Jfc1gmX12iX1Ku3q95mn9V3S6nmW5vdimjp83VPIY8EfAjzFh1-JfGuzQXMvDLlOaX7NmIsYRXx37Kvl9e3HQf6-vPH6668-vaKyWhRi102zcDWqvkIK1Ca1D0HoTiWo2j7lsFvecSrB51QN0PSFLT2rYZVM_lKXt38L3N6W4NZXH7qfgQI84hrcWZFqyhUAg8O4A-p1JyGN1tnvaY_zkO7iFMB9xRmE4LR2UsTbw5Wq_9PgyP_DE90t8edSwe45hx9lN5xEwjlZAPD6sDdp_iEnL5E9f7kN0uYFx2jv4IJHBRc9u2IOhU0-Ig_wNmV4tB</recordid><startdate>198802</startdate><enddate>198802</enddate><creator>Paganelli, William C</creator><creator>Cant, James R</creator><creator>Pintal, Richard R</creator><creator>A, Imre Kifor</creator><creator>Barger, Clifford</creator><creator>Dzau, Victor J</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>198802</creationdate><title>Plasma Atrial Natriuretic Factor During Chronic Thoracic Inferior Vena Caval Constriction</title><author>Paganelli, William C ; Cant, James R ; Pintal, Richard R ; A, Imre Kifor ; Barger, Clifford ; Dzau, Victor J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4430-a6268b5da9943d394a97a2bc024164ff6b840bc13096f6ea6bda24158985d4b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Animals</topic><topic>Arginine Vasopressin - blood</topic><topic>Atrial Natriuretic Factor - blood</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure</topic><topic>Cardiology. Vascular system</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Dogs</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Renin - blood</topic><topic>Sodium - metabolism</topic><topic>Vasoconstriction</topic><topic>Vena Cava, Inferior - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Paganelli, William C</creatorcontrib><creatorcontrib>Cant, James R</creatorcontrib><creatorcontrib>Pintal, Richard R</creatorcontrib><creatorcontrib>A, Imre Kifor</creatorcontrib><creatorcontrib>Barger, Clifford</creatorcontrib><creatorcontrib>Dzau, Victor J</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>Paganelli, William C</au><au>Cant, James R</au><au>Pintal, Richard R</au><au>A, Imre Kifor</au><au>Barger, Clifford</au><au>Dzau, Victor J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasma Atrial Natriuretic Factor During Chronic Thoracic Inferior Vena Caval Constriction</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1988-02</date><risdate>1988</risdate><volume>62</volume><issue>2</issue><spage>279</spage><epage>285</epage><pages>279-285</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>The effects of chronic constriction of the thoracic inferior vena cava (TIVCC) on plasma atrial natriuretic factor (pANF) were studied in conscious dogs (n = 5). TIVCC decreased left and right atria] pressure and led to a decrease in pANF concentration from 199 ± 12 to 104 ± 14 pg/ml while plasma renin and vasopressin concentrations increased. These hormonal changes were associated with a significant fall in sodium excretion to &lt;5 meq/day. pANF remained suppressed during chronic TIVCC as the dogs expanded their extracellular fluid volume and developed ascites. Acute release of TIVCC resulted in abrupt increases in left and right atrial pressure but only a modest rise in pANF from 96 ± 16 to 185 ± 45 pg/ml. The magnitude of the rise in pANF (twofold) contrasted sharply with the eightfold increase in sodium excretion that occurred over the first 24 hours. Our data suggest that decrease in atrial pressure below normal results in a decline in pANF, which, acting in concert with the activated renin-angiotensin system and vasopressin, may contribute to sodium retention. On the other hand, during acute release of TIVCC, which markedly increased atrial pressure and sodium excretion, pANF only returned to control levels. These data suggest that ANF release may be attenuated during chronic reduction in atrial pressure and also raise a question concerning the magnitude of the primary role of ANF in this natriuretic response.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>2962784</pmid><doi>10.1161/01.RES.62.2.279</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0009-7330
ispartof Circulation research, 1988-02, Vol.62 (2), p.279-285
issn 0009-7330
1524-4571
language eng
recordid cdi_proquest_miscellaneous_78097152
source Freely Accessible Science Journals
subjects Animals
Arginine Vasopressin - blood
Atrial Natriuretic Factor - blood
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure
Cardiology. Vascular system
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Dogs
Male
Medical sciences
Renin - blood
Sodium - metabolism
Vasoconstriction
Vena Cava, Inferior - physiology
title Plasma Atrial Natriuretic Factor During Chronic Thoracic Inferior Vena Caval Constriction
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T15%3A39%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Plasma%20Atrial%20Natriuretic%20Factor%20During%20Chronic%20Thoracic%20Inferior%20Vena%20Caval%20Constriction&rft.jtitle=Circulation%20research&rft.au=Paganelli,%20William%20C&rft.date=1988-02&rft.volume=62&rft.issue=2&rft.spage=279&rft.epage=285&rft.pages=279-285&rft.issn=0009-7330&rft.eissn=1524-4571&rft.coden=CIRUAL&rft_id=info:doi/10.1161/01.RES.62.2.279&rft_dat=%3Cproquest_cross%3E78097152%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4430-a6268b5da9943d394a97a2bc024164ff6b840bc13096f6ea6bda24158985d4b13%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=78097152&rft_id=info:pmid/2962784&rfr_iscdi=true