Blunted systemic, splanchnic, and renal hemodynamic responses to atrial natriuretic peptide in rats with cirrhosis
Systemic, splanchnic and renal hemodynamic responses to saline, physiological (25 ng·kg −1·min −1) and pharmacological (100, 300 and 600 ng·kg −1·min −1) doses of α human atrial natriuretic peptide were measured in normal ( n=7 for saline and 7–8 for each dose of atrial natriuretic peptide) and cirr...
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| Veröffentlicht in: | Journal of hepatology 1994, Vol.20 (1), p.91-96 |
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| creator | Ohsuga, Masaru Moreau, Richard Hartleb, Marek Komeichi, Hirokazu Lebrec, Didier |
| description | Systemic, splanchnic and renal hemodynamic responses to saline, physiological (25 ng·kg
−1·min
−1) and pharmacological (100, 300 and 600 ng·kg
−1·min
−1) doses of
α human atrial natriuretic peptide were measured in normal (
n=7 for saline and 7–8 for each dose of atrial natriuretic peptide) and cirrhotic (
n=7 for saline and 7–8 for each dose of atrial natriuretic peptide), conscious, unrestrained rats. In addition, plasma norepinephrine concentrations were measured in normal and cirrhotic rats, before and following a 300-ng·kg
−1·min
−1 dose of atrial natriuretic peptide. In cirrhotic rats, splanchnic, renal and systemic hemodynamics were not significantly affected by either physiological or pharmacological doses of atrial natriuretic peptide. In normal rats, a 300 ng·kg
−1·min
−1 dose of atrial natriuretic peptide significantly decreased cardiac index, portal tributary blood flow and renal blood flow, and significantly increased vascular resistance in the systemic, portal, and renal territories. The other doses of atrial natriuretic peptide did not significantly change regional and systemic hemodynamics. Atrial natriuretic peptide-induced changes in plasma norepinephrine concentrations were significantly higher in normal than in cirrhotic rats (1827±834 vs. 59±46 pg/ml, mean±S.E., respectively). In conclusion, this study shows that the normal cardiovascular response to a 300 ng·kg
−1·min
−1 atrial natriuretic peptide infusion is blunted in cirrhotic rats. Moreover, in cirrhotic rats, blunting of vasoconstriction following atrial natriuretic peptide administration seems to be due to a lack of increased sympathetic vascular tone. |
| doi_str_mv | 10.1016/S0168-8278(05)80472-6 |
| format | Article |
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−1·min
−1) and pharmacological (100, 300 and 600 ng·kg
−1·min
−1) doses of
α human atrial natriuretic peptide were measured in normal (
n=7 for saline and 7–8 for each dose of atrial natriuretic peptide) and cirrhotic (
n=7 for saline and 7–8 for each dose of atrial natriuretic peptide), conscious, unrestrained rats. In addition, plasma norepinephrine concentrations were measured in normal and cirrhotic rats, before and following a 300-ng·kg
−1·min
−1 dose of atrial natriuretic peptide. In cirrhotic rats, splanchnic, renal and systemic hemodynamics were not significantly affected by either physiological or pharmacological doses of atrial natriuretic peptide. In normal rats, a 300 ng·kg
−1·min
−1 dose of atrial natriuretic peptide significantly decreased cardiac index, portal tributary blood flow and renal blood flow, and significantly increased vascular resistance in the systemic, portal, and renal territories. The other doses of atrial natriuretic peptide did not significantly change regional and systemic hemodynamics. Atrial natriuretic peptide-induced changes in plasma norepinephrine concentrations were significantly higher in normal than in cirrhotic rats (1827±834 vs. 59±46 pg/ml, mean±S.E., respectively). In conclusion, this study shows that the normal cardiovascular response to a 300 ng·kg
−1·min
−1 atrial natriuretic peptide infusion is blunted in cirrhotic rats. Moreover, in cirrhotic rats, blunting of vasoconstriction following atrial natriuretic peptide administration seems to be due to a lack of increased sympathetic vascular tone.</description><identifier>ISSN: 0168-8278</identifier><identifier>EISSN: 1600-0641</identifier><identifier>DOI: 10.1016/S0168-8278(05)80472-6</identifier><identifier>PMID: 8201228</identifier><identifier>CODEN: JOHEEC</identifier><language>eng</language><publisher>Oxford: Elsevier B.V</publisher><subject>Animals ; Atrial Natriuretic Factor - pharmacology ; Biological and medical sciences ; Cardiac output ; Diuretics - pharmacology ; Dose-Response Relationship, Drug ; Gastroenterology. Liver. Pancreas. Abdomen ; Hemodynamics - drug effects ; Liver Cirrhosis, Experimental - physiopathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Norepinephrine - blood ; Other diseases. Semiology ; Peptide Fragments - pharmacology ; Portal hypertension ; Portal pressure ; Radioactive microspheres ; Rats ; Rats, Sprague-Dawley ; Renal Circulation - drug effects ; Sodium Chloride - pharmacology ; Splanchnic blood flow ; Splanchnic Circulation - drug effects</subject><ispartof>Journal of hepatology, 1994, Vol.20 (1), p.91-96</ispartof><rights>1994 Journal of Hepatology</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-656c819f71c7cca6150ffb3c54ad310b08aeb99f2cd67392a8c71e9864788ec03</citedby><cites>FETCH-LOGICAL-c389t-656c819f71c7cca6150ffb3c54ad310b08aeb99f2cd67392a8c71e9864788ec03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0168-8278(05)80472-6$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3940173$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8201228$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ohsuga, Masaru</creatorcontrib><creatorcontrib>Moreau, Richard</creatorcontrib><creatorcontrib>Hartleb, Marek</creatorcontrib><creatorcontrib>Komeichi, Hirokazu</creatorcontrib><creatorcontrib>Lebrec, Didier</creatorcontrib><title>Blunted systemic, splanchnic, and renal hemodynamic responses to atrial natriuretic peptide in rats with cirrhosis</title><title>Journal of hepatology</title><addtitle>J Hepatol</addtitle><description>Systemic, splanchnic and renal hemodynamic responses to saline, physiological (25 ng·kg
−1·min
−1) and pharmacological (100, 300 and 600 ng·kg
−1·min
−1) doses of
α human atrial natriuretic peptide were measured in normal (
n=7 for saline and 7–8 for each dose of atrial natriuretic peptide) and cirrhotic (
n=7 for saline and 7–8 for each dose of atrial natriuretic peptide), conscious, unrestrained rats. In addition, plasma norepinephrine concentrations were measured in normal and cirrhotic rats, before and following a 300-ng·kg
−1·min
−1 dose of atrial natriuretic peptide. In cirrhotic rats, splanchnic, renal and systemic hemodynamics were not significantly affected by either physiological or pharmacological doses of atrial natriuretic peptide. In normal rats, a 300 ng·kg
−1·min
−1 dose of atrial natriuretic peptide significantly decreased cardiac index, portal tributary blood flow and renal blood flow, and significantly increased vascular resistance in the systemic, portal, and renal territories. The other doses of atrial natriuretic peptide did not significantly change regional and systemic hemodynamics. Atrial natriuretic peptide-induced changes in plasma norepinephrine concentrations were significantly higher in normal than in cirrhotic rats (1827±834 vs. 59±46 pg/ml, mean±S.E., respectively). In conclusion, this study shows that the normal cardiovascular response to a 300 ng·kg
−1·min
−1 atrial natriuretic peptide infusion is blunted in cirrhotic rats. Moreover, in cirrhotic rats, blunting of vasoconstriction following atrial natriuretic peptide administration seems to be due to a lack of increased sympathetic vascular tone.</description><subject>Animals</subject><subject>Atrial Natriuretic Factor - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cardiac output</subject><subject>Diuretics - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hemodynamics - drug effects</subject><subject>Liver Cirrhosis, Experimental - physiopathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Norepinephrine - blood</subject><subject>Other diseases. Semiology</subject><subject>Peptide Fragments - pharmacology</subject><subject>Portal hypertension</subject><subject>Portal pressure</subject><subject>Radioactive microspheres</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renal Circulation - drug effects</subject><subject>Sodium Chloride - pharmacology</subject><subject>Splanchnic blood flow</subject><subject>Splanchnic Circulation - drug effects</subject><issn>0168-8278</issn><issn>1600-0641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFu1DAQhi1EVZbCI1TyASGQCIzjxHZOCCqglSpxAM6W15lojRIneByqfXu83dVeuXgs_9-M7Y-xawHvBQj14UdZTGVqbd5A-9ZAo-tKPWEboQAqUI14yjZn5Bl7TvQbACR0zSW7NDWIujYblj6Pa8zYc9pTxin4d5yW0UW_i4e9iz1PGN3IdzjN_T66gpQTWuZISDzP3OUUSh4PdU2YS77gkkOPPESeXCb-EPKO-5DSbqZAL9jF4EbCl6d6xX59_fLz5ra6__7t7ubTfeWl6XKlWuWN6AYtvPbeKdHCMGylbxvXSwFbMA63XTfUvldadrUzXgvsjGq0MehBXrHXx7lLmv-sSNlOgTyO5Xc4r2S1aqUwUhSwPYI-zUQJB7ukMLm0twLswbV9dG0PIi209tG1VaXv-nTBup2wP3ed5Jb81Sl35N04pKI10BmTXQNCy4J9PGJYZPwNmCz5gNFjHxL6bPs5_Och_wCLop0U</recordid><startdate>1994</startdate><enddate>1994</enddate><creator>Ohsuga, Masaru</creator><creator>Moreau, Richard</creator><creator>Hartleb, Marek</creator><creator>Komeichi, Hirokazu</creator><creator>Lebrec, Didier</creator><general>Elsevier B.V</general><general>Elsevier</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>1994</creationdate><title>Blunted systemic, splanchnic, and renal hemodynamic responses to atrial natriuretic peptide in rats with cirrhosis</title><author>Ohsuga, Masaru ; Moreau, Richard ; Hartleb, Marek ; Komeichi, Hirokazu ; Lebrec, Didier</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-656c819f71c7cca6150ffb3c54ad310b08aeb99f2cd67392a8c71e9864788ec03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Atrial Natriuretic Factor - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cardiac output</topic><topic>Diuretics - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hemodynamics - drug effects</topic><topic>Liver Cirrhosis, Experimental - physiopathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Norepinephrine - blood</topic><topic>Other diseases. Semiology</topic><topic>Peptide Fragments - pharmacology</topic><topic>Portal hypertension</topic><topic>Portal pressure</topic><topic>Radioactive microspheres</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renal Circulation - drug effects</topic><topic>Sodium Chloride - pharmacology</topic><topic>Splanchnic blood flow</topic><topic>Splanchnic Circulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ohsuga, Masaru</creatorcontrib><creatorcontrib>Moreau, Richard</creatorcontrib><creatorcontrib>Hartleb, Marek</creatorcontrib><creatorcontrib>Komeichi, Hirokazu</creatorcontrib><creatorcontrib>Lebrec, Didier</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>Journal of hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ohsuga, Masaru</au><au>Moreau, Richard</au><au>Hartleb, Marek</au><au>Komeichi, Hirokazu</au><au>Lebrec, Didier</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Blunted systemic, splanchnic, and renal hemodynamic responses to atrial natriuretic peptide in rats with cirrhosis</atitle><jtitle>Journal of hepatology</jtitle><addtitle>J Hepatol</addtitle><date>1994</date><risdate>1994</risdate><volume>20</volume><issue>1</issue><spage>91</spage><epage>96</epage><pages>91-96</pages><issn>0168-8278</issn><eissn>1600-0641</eissn><coden>JOHEEC</coden><abstract>Systemic, splanchnic and renal hemodynamic responses to saline, physiological (25 ng·kg
−1·min
−1) and pharmacological (100, 300 and 600 ng·kg
−1·min
−1) doses of
α human atrial natriuretic peptide were measured in normal (
n=7 for saline and 7–8 for each dose of atrial natriuretic peptide) and cirrhotic (
n=7 for saline and 7–8 for each dose of atrial natriuretic peptide), conscious, unrestrained rats. In addition, plasma norepinephrine concentrations were measured in normal and cirrhotic rats, before and following a 300-ng·kg
−1·min
−1 dose of atrial natriuretic peptide. In cirrhotic rats, splanchnic, renal and systemic hemodynamics were not significantly affected by either physiological or pharmacological doses of atrial natriuretic peptide. In normal rats, a 300 ng·kg
−1·min
−1 dose of atrial natriuretic peptide significantly decreased cardiac index, portal tributary blood flow and renal blood flow, and significantly increased vascular resistance in the systemic, portal, and renal territories. The other doses of atrial natriuretic peptide did not significantly change regional and systemic hemodynamics. Atrial natriuretic peptide-induced changes in plasma norepinephrine concentrations were significantly higher in normal than in cirrhotic rats (1827±834 vs. 59±46 pg/ml, mean±S.E., respectively). In conclusion, this study shows that the normal cardiovascular response to a 300 ng·kg
−1·min
−1 atrial natriuretic peptide infusion is blunted in cirrhotic rats. Moreover, in cirrhotic rats, blunting of vasoconstriction following atrial natriuretic peptide administration seems to be due to a lack of increased sympathetic vascular tone.</abstract><cop>Oxford</cop><pub>Elsevier B.V</pub><pmid>8201228</pmid><doi>10.1016/S0168-8278(05)80472-6</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0168-8278 |
| ispartof | Journal of hepatology, 1994, Vol.20 (1), p.91-96 |
| issn | 0168-8278 1600-0641 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_76531831 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Animals Atrial Natriuretic Factor - pharmacology Biological and medical sciences Cardiac output Diuretics - pharmacology Dose-Response Relationship, Drug Gastroenterology. Liver. Pancreas. Abdomen Hemodynamics - drug effects Liver Cirrhosis, Experimental - physiopathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Norepinephrine - blood Other diseases. Semiology Peptide Fragments - pharmacology Portal hypertension Portal pressure Radioactive microspheres Rats Rats, Sprague-Dawley Renal Circulation - drug effects Sodium Chloride - pharmacology Splanchnic blood flow Splanchnic Circulation - drug effects |
| title | Blunted systemic, splanchnic, and renal hemodynamic responses to atrial natriuretic peptide in rats with cirrhosis |
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