Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: The effect of acute plasma expansion
Twenty cirrhotic patients with ascites, divided into two groups of 10 each, according to their daily urinary sodium excretion (sodium retainers and sodium excretors) and given a diet of 75 mEq of sodium daily, underwent acute plasma volume expansion with 1,000 ml of 10% dextran in saline, infused th...
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| Veröffentlicht in: | Pharmacological research communications 1984-06, Vol.16 (6), p.613-635 |
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| creator | Laffi, Giacomo La Villa, Giorgio Pinzani, Massimo Mannelli, Massimo Buzzelli, Giampiero Paladini, Sergio Pampana, Alessandro Smorlesi, Carlo Pedretti, Giorgio Gentilini, Paolo |
| description | Twenty cirrhotic patients with ascites, divided into two groups of 10 each, according to their daily urinary sodium excretion (sodium retainers and sodium excretors) and given a diet of 75 mEq of sodium daily, underwent acute plasma volume expansion with 1,000 ml of 10% dextran in saline, infused through a catheter located in the right atrium.
Even if a significant increase in sodium excretion was observed in both groups (p < 0.001 in sodium excretors and p < 0.05 in sodium retainers), plasma expansion did not reverse sodium retention in sodium retainers.
A significant increase in creatinine clearance was found only in sodium retainers (p < 0.02). Basal plasma renin activity and plasma aldosterone were elevated only in a few patients of both groups. The renin-angiotensin-aldosterone system was highly responsive to plasma expansion. Sodium retainers, who showed an ineffective natriuretic response after expansion, were able to suppress both plasma renin activity and plasma aldosterone in an analogous manner to the sodium-excreting group. This result lends strong support to the concept that the elevated aldosterone level in cirrhosis is not the major determinant of sodium retention.
The kallikrein-kinin system was responsive to volume stimulus, since a decrease in kallikrein excretion was noted. It was significant in sodium retainers (p < 0.05). Plasma PGE
1,2 levels were significantly higher in sodium retainers than in controls. This may suggest that there is an activation of the intrarenal prostaglandin system, which could play a protective role against renal ischaemia. After volume expansion, PGE
1,2 increased, but not significantly. Octopamine appeared unrelated to sodium excretion and unresponsive to volume stimulus. Endotoxins did not seem to be involved in renal sodium handling.
Plasma volume expansion seemed effective in inducing a reduction of vasoconstrictor and sodium-retaining factors, such as the renin-angiotensin-aldosterone system. It is possible to suggest that volume expansion could increase PGE
1,2. Plasma volume expansion produced different rates of sodium excretion in the two groups of patients and this suggests that impaired sodium handling in cirrhosis could, to some extent, be independent of effective plasma volume. |
| doi_str_mv | 10.1016/S0031-6989(84)80041-7 |
| format | Article |
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Even if a significant increase in sodium excretion was observed in both groups (p < 0.001 in sodium excretors and p < 0.05 in sodium retainers), plasma expansion did not reverse sodium retention in sodium retainers.
A significant increase in creatinine clearance was found only in sodium retainers (p < 0.02). Basal plasma renin activity and plasma aldosterone were elevated only in a few patients of both groups. The renin-angiotensin-aldosterone system was highly responsive to plasma expansion. Sodium retainers, who showed an ineffective natriuretic response after expansion, were able to suppress both plasma renin activity and plasma aldosterone in an analogous manner to the sodium-excreting group. This result lends strong support to the concept that the elevated aldosterone level in cirrhosis is not the major determinant of sodium retention.
The kallikrein-kinin system was responsive to volume stimulus, since a decrease in kallikrein excretion was noted. It was significant in sodium retainers (p < 0.05). Plasma PGE
1,2 levels were significantly higher in sodium retainers than in controls. This may suggest that there is an activation of the intrarenal prostaglandin system, which could play a protective role against renal ischaemia. After volume expansion, PGE
1,2 increased, but not significantly. Octopamine appeared unrelated to sodium excretion and unresponsive to volume stimulus. Endotoxins did not seem to be involved in renal sodium handling.
Plasma volume expansion seemed effective in inducing a reduction of vasoconstrictor and sodium-retaining factors, such as the renin-angiotensin-aldosterone system. It is possible to suggest that volume expansion could increase PGE
1,2. Plasma volume expansion produced different rates of sodium excretion in the two groups of patients and this suggests that impaired sodium handling in cirrhosis could, to some extent, be independent of effective plasma volume.</description><identifier>ISSN: 0031-6989</identifier><identifier>EISSN: 1879-2936</identifier><identifier>DOI: 10.1016/S0031-6989(84)80041-7</identifier><identifier>PMID: 6431453</identifier><language>eng</language><publisher>Orlando, FL: Elsevier B.V</publisher><subject>Biological and medical sciences ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Kallikreins - urine ; Kidney Function Tests ; Liver Cirrhosis - physiopathology ; Liver Cirrhosis - therapy ; Liver Cirrhosis - urine ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Middle Aged ; Octopamine - blood ; Other diseases. Semiology ; Plasma Substitutes - administration & dosage ; Plasma Volume ; Potassium - urine ; Prostaglandins E - blood ; Renin-Angiotensin System ; Sodium - urine</subject><ispartof>Pharmacological research communications, 1984-06, Vol.16 (6), p.613-635</ispartof><rights>1984 The Italian Pharmacological Society</rights><rights>1985 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-a4ae43eef39f29dbe8e8bd8f2415a8f01fe06250b7db59eb03075e6ad1cdb5fd3</citedby><cites>FETCH-LOGICAL-c389t-a4ae43eef39f29dbe8e8bd8f2415a8f01fe06250b7db59eb03075e6ad1cdb5fd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27928,27929</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8910701$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6431453$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Laffi, Giacomo</creatorcontrib><creatorcontrib>La Villa, Giorgio</creatorcontrib><creatorcontrib>Pinzani, Massimo</creatorcontrib><creatorcontrib>Mannelli, Massimo</creatorcontrib><creatorcontrib>Buzzelli, Giampiero</creatorcontrib><creatorcontrib>Paladini, Sergio</creatorcontrib><creatorcontrib>Pampana, Alessandro</creatorcontrib><creatorcontrib>Smorlesi, Carlo</creatorcontrib><creatorcontrib>Pedretti, Giorgio</creatorcontrib><creatorcontrib>Gentilini, Paolo</creatorcontrib><title>Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: The effect of acute plasma expansion</title><title>Pharmacological research communications</title><addtitle>Pharmacol Res Commun</addtitle><description>Twenty cirrhotic patients with ascites, divided into two groups of 10 each, according to their daily urinary sodium excretion (sodium retainers and sodium excretors) and given a diet of 75 mEq of sodium daily, underwent acute plasma volume expansion with 1,000 ml of 10% dextran in saline, infused through a catheter located in the right atrium.
Even if a significant increase in sodium excretion was observed in both groups (p < 0.001 in sodium excretors and p < 0.05 in sodium retainers), plasma expansion did not reverse sodium retention in sodium retainers.
A significant increase in creatinine clearance was found only in sodium retainers (p < 0.02). Basal plasma renin activity and plasma aldosterone were elevated only in a few patients of both groups. The renin-angiotensin-aldosterone system was highly responsive to plasma expansion. Sodium retainers, who showed an ineffective natriuretic response after expansion, were able to suppress both plasma renin activity and plasma aldosterone in an analogous manner to the sodium-excreting group. This result lends strong support to the concept that the elevated aldosterone level in cirrhosis is not the major determinant of sodium retention.
The kallikrein-kinin system was responsive to volume stimulus, since a decrease in kallikrein excretion was noted. It was significant in sodium retainers (p < 0.05). Plasma PGE
1,2 levels were significantly higher in sodium retainers than in controls. This may suggest that there is an activation of the intrarenal prostaglandin system, which could play a protective role against renal ischaemia. After volume expansion, PGE
1,2 increased, but not significantly. Octopamine appeared unrelated to sodium excretion and unresponsive to volume stimulus. Endotoxins did not seem to be involved in renal sodium handling.
Plasma volume expansion seemed effective in inducing a reduction of vasoconstrictor and sodium-retaining factors, such as the renin-angiotensin-aldosterone system. It is possible to suggest that volume expansion could increase PGE
1,2. Plasma volume expansion produced different rates of sodium excretion in the two groups of patients and this suggests that impaired sodium handling in cirrhosis could, to some extent, be independent of effective plasma volume.</description><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Kallikreins - urine</subject><subject>Kidney Function Tests</subject><subject>Liver Cirrhosis - physiopathology</subject><subject>Liver Cirrhosis - therapy</subject><subject>Liver Cirrhosis - urine</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Octopamine - blood</subject><subject>Other diseases. Semiology</subject><subject>Plasma Substitutes - administration & dosage</subject><subject>Plasma Volume</subject><subject>Potassium - urine</subject><subject>Prostaglandins E - blood</subject><subject>Renin-Angiotensin System</subject><subject>Sodium - urine</subject><issn>0031-6989</issn><issn>1879-2936</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE2LFDEQhoMo67j6ExZyENFDa9JJdydeRBa_YMGDq9dQnVScSHfSJt2L_nszO8NcPRVV9byV8BByxdlrznj_5htjgje9Vvqlkq8UY5I3wwOy42rQTatF_5Dszshj8qSUX7Vte84uyEUvBZed2JHlB5QEdg13SH2tKRcaIl33SGe0e4ihzDR5mjHCREtyYZtpHbspxJ8H0oac92kNtryltzWF3qNdDxGw24p0maDMQPHPArGEFJ-SRx6mgs9O9ZJ8__jh9vpzc_P105fr9zeNFUqvDUhAKRC90L7VbkSFanTKt5J3oDzjHlnfdmwc3NhpHJlgQ4c9OG7rwDtxSV4c7y45_d6wrGYOxeI0QcS0FaM4V90gdQW7I2hzKiWjN0sOM-S_hjNzMG3uTZuDRqOkuTdthpq7Oj2wjTO6c-qktu6fn_ZQLEw-Q7ShnDGlORsYr9i7I4ZVxl3AbIoNGC26kKtI41L4z0f-ATponL8</recordid><startdate>198406</startdate><enddate>198406</enddate><creator>Laffi, Giacomo</creator><creator>La Villa, Giorgio</creator><creator>Pinzani, Massimo</creator><creator>Mannelli, Massimo</creator><creator>Buzzelli, Giampiero</creator><creator>Paladini, Sergio</creator><creator>Pampana, Alessandro</creator><creator>Smorlesi, Carlo</creator><creator>Pedretti, Giorgio</creator><creator>Gentilini, Paolo</creator><general>Elsevier B.V</general><general>Academic Press</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>198406</creationdate><title>Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: The effect of acute plasma expansion</title><author>Laffi, Giacomo ; La Villa, Giorgio ; Pinzani, Massimo ; Mannelli, Massimo ; Buzzelli, Giampiero ; Paladini, Sergio ; Pampana, Alessandro ; Smorlesi, Carlo ; Pedretti, Giorgio ; Gentilini, Paolo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-a4ae43eef39f29dbe8e8bd8f2415a8f01fe06250b7db59eb03075e6ad1cdb5fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Biological and medical sciences</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Kallikreins - urine</topic><topic>Kidney Function Tests</topic><topic>Liver Cirrhosis - physiopathology</topic><topic>Liver Cirrhosis - therapy</topic><topic>Liver Cirrhosis - urine</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Octopamine - blood</topic><topic>Other diseases. Semiology</topic><topic>Plasma Substitutes - administration & dosage</topic><topic>Plasma Volume</topic><topic>Potassium - urine</topic><topic>Prostaglandins E - blood</topic><topic>Renin-Angiotensin System</topic><topic>Sodium - urine</topic><toplevel>online_resources</toplevel><creatorcontrib>Laffi, Giacomo</creatorcontrib><creatorcontrib>La Villa, Giorgio</creatorcontrib><creatorcontrib>Pinzani, Massimo</creatorcontrib><creatorcontrib>Mannelli, Massimo</creatorcontrib><creatorcontrib>Buzzelli, Giampiero</creatorcontrib><creatorcontrib>Paladini, Sergio</creatorcontrib><creatorcontrib>Pampana, Alessandro</creatorcontrib><creatorcontrib>Smorlesi, Carlo</creatorcontrib><creatorcontrib>Pedretti, Giorgio</creatorcontrib><creatorcontrib>Gentilini, Paolo</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>Pharmacological research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Laffi, Giacomo</au><au>La Villa, Giorgio</au><au>Pinzani, Massimo</au><au>Mannelli, Massimo</au><au>Buzzelli, Giampiero</au><au>Paladini, Sergio</au><au>Pampana, Alessandro</au><au>Smorlesi, Carlo</au><au>Pedretti, Giorgio</au><au>Gentilini, Paolo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: The effect of acute plasma expansion</atitle><jtitle>Pharmacological research communications</jtitle><addtitle>Pharmacol Res Commun</addtitle><date>1984-06</date><risdate>1984</risdate><volume>16</volume><issue>6</issue><spage>613</spage><epage>635</epage><pages>613-635</pages><issn>0031-6989</issn><eissn>1879-2936</eissn><abstract>Twenty cirrhotic patients with ascites, divided into two groups of 10 each, according to their daily urinary sodium excretion (sodium retainers and sodium excretors) and given a diet of 75 mEq of sodium daily, underwent acute plasma volume expansion with 1,000 ml of 10% dextran in saline, infused through a catheter located in the right atrium.
Even if a significant increase in sodium excretion was observed in both groups (p < 0.001 in sodium excretors and p < 0.05 in sodium retainers), plasma expansion did not reverse sodium retention in sodium retainers.
A significant increase in creatinine clearance was found only in sodium retainers (p < 0.02). Basal plasma renin activity and plasma aldosterone were elevated only in a few patients of both groups. The renin-angiotensin-aldosterone system was highly responsive to plasma expansion. Sodium retainers, who showed an ineffective natriuretic response after expansion, were able to suppress both plasma renin activity and plasma aldosterone in an analogous manner to the sodium-excreting group. This result lends strong support to the concept that the elevated aldosterone level in cirrhosis is not the major determinant of sodium retention.
The kallikrein-kinin system was responsive to volume stimulus, since a decrease in kallikrein excretion was noted. It was significant in sodium retainers (p < 0.05). Plasma PGE
1,2 levels were significantly higher in sodium retainers than in controls. This may suggest that there is an activation of the intrarenal prostaglandin system, which could play a protective role against renal ischaemia. After volume expansion, PGE
1,2 increased, but not significantly. Octopamine appeared unrelated to sodium excretion and unresponsive to volume stimulus. Endotoxins did not seem to be involved in renal sodium handling.
Plasma volume expansion seemed effective in inducing a reduction of vasoconstrictor and sodium-retaining factors, such as the renin-angiotensin-aldosterone system. It is possible to suggest that volume expansion could increase PGE
1,2. Plasma volume expansion produced different rates of sodium excretion in the two groups of patients and this suggests that impaired sodium handling in cirrhosis could, to some extent, be independent of effective plasma volume.</abstract><cop>Orlando, FL</cop><cop>London</cop><pub>Elsevier B.V</pub><pmid>6431453</pmid><doi>10.1016/S0031-6989(84)80041-7</doi><tpages>23</tpages></addata></record> |
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| ispartof | Pharmacological research communications, 1984-06, Vol.16 (6), p.613-635 |
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| subjects | Biological and medical sciences Female Gastroenterology. Liver. Pancreas. Abdomen Humans Kallikreins - urine Kidney Function Tests Liver Cirrhosis - physiopathology Liver Cirrhosis - therapy Liver Cirrhosis - urine Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Middle Aged Octopamine - blood Other diseases. Semiology Plasma Substitutes - administration & dosage Plasma Volume Potassium - urine Prostaglandins E - blood Renin-Angiotensin System Sodium - urine |
| title | Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: The effect of acute plasma expansion |
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