HUMORAL DETERMINANTS OF Na+ EXCRETION AFTER INTRAVENOUS NaCl LOADING IN NORMAL VOLUNTEERS
SUMMARY 1. Twelve healthy volunteers maintained on a 100 mmol/day Na+ diet, were given an intravenous infusion of 2L saline (0.9%) between 10.00 and 13.00h on 2 study days at least 1 week apart. Urine collections (90 min) were made from 08.30 to 16.00 h. Either carbidopa 100 mg or indomethacin 50 mg...
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| Veröffentlicht in: | Clinical and experimental pharmacology & physiology 1993-05, Vol.20 (5), p.310-312 |
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| creator | Stokes, G. S. Johnston, H. J. Monaghan, J. C. |
| description | SUMMARY
1. Twelve healthy volunteers maintained on a 100 mmol/day Na+ diet, were given an intravenous infusion of 2L saline (0.9%) between 10.00 and 13.00h on 2 study days at least 1 week apart. Urine collections (90 min) were made from 08.30 to 16.00 h. Either carbidopa 100 mg or indomethacin 50 mg was given orally at 07.45 h on one study day and placebo was given on the other (in random order).
2. On the placebo day, saline infusion caused significant decreases in plasma albumin concentration, plasma renin activity (PRA), plasma aldosterone concentration and urinary aldosterone excretion, with 2 to 3‐fold increases in plasma atrial natriuretic peptide (ANP) concentration and urinary dopamine: noradrenaline ratio (DA:NA), whereas mean urinary kallikrein and prostaglandin E2 (PGEI) excretion rates were unchanged. Carbidopa decreased urinary DA:NA and indomethacin decreased urinary PGE2 excretion, compared with the placebo day. Excretion of sodium (Na+) decreased below baseline in two out of six carbidopa‐treated subjects and in three out of six indomethacin‐treated subjects, but showed little or no change in the remainder.
3. These preliminary observations suggest that some subjects in the early phase of natriuresis after an intravenous Na+ load can be identified as having prostaglandin‐dependent or dopamine‐dependent mechanisms for Na+ excretion. |
| doi_str_mv | 10.1111/j.1440-1681.1993.tb01691.x |
| format | Article |
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1. Twelve healthy volunteers maintained on a 100 mmol/day Na+ diet, were given an intravenous infusion of 2L saline (0.9%) between 10.00 and 13.00h on 2 study days at least 1 week apart. Urine collections (90 min) were made from 08.30 to 16.00 h. Either carbidopa 100 mg or indomethacin 50 mg was given orally at 07.45 h on one study day and placebo was given on the other (in random order).
2. On the placebo day, saline infusion caused significant decreases in plasma albumin concentration, plasma renin activity (PRA), plasma aldosterone concentration and urinary aldosterone excretion, with 2 to 3‐fold increases in plasma atrial natriuretic peptide (ANP) concentration and urinary dopamine: noradrenaline ratio (DA:NA), whereas mean urinary kallikrein and prostaglandin E2 (PGEI) excretion rates were unchanged. Carbidopa decreased urinary DA:NA and indomethacin decreased urinary PGE2 excretion, compared with the placebo day. Excretion of sodium (Na+) decreased below baseline in two out of six carbidopa‐treated subjects and in three out of six indomethacin‐treated subjects, but showed little or no change in the remainder.
3. These preliminary observations suggest that some subjects in the early phase of natriuresis after an intravenous Na+ load can be identified as having prostaglandin‐dependent or dopamine‐dependent mechanisms for Na+ excretion.</description><identifier>ISSN: 0305-1870</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1111/j.1440-1681.1993.tb01691.x</identifier><identifier>PMID: 8324915</identifier><identifier>CODEN: CEXPB9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Adult ; aldosterone ; Aldosterone - blood ; Aldosterone - urine ; Atrial Natriuretic Factor - blood ; atrial natriuretic peptide ; Biological and medical sciences ; carbidopa ; Carbidopa - administration & dosage ; Carbidopa - pharmacology ; Dopamine - urine ; doparnine ; excretion ; Female ; Fundamental and applied biological sciences. Psychology ; Hemodynamics. Rheology ; Humans ; Indomethacin - administration & dosage ; Indomethacin - pharmacology ; indornethacin ; kallikrein ; Kallikreins - urine ; Male ; Middle Aged ; Na+ ; Natriuresis - drug effects ; Norepinephrine - urine ; prostaglandins ; Prostaglandins - urine ; Prostaglandins E - urine ; renin ; Renin - blood ; Serum Albumin - analysis ; Sodium - administration & dosage ; Sodium - urine ; Vertebrates: cardiovascular system</subject><ispartof>Clinical and experimental pharmacology & physiology, 1993-05, Vol.20 (5), p.310-312</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4360-d437f00cf24a8723dd10155d358096a447e18e630e6b98da4a4995f9633876e03</citedby><cites>FETCH-LOGICAL-c4360-d437f00cf24a8723dd10155d358096a447e18e630e6b98da4a4995f9633876e03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1440-1681.1993.tb01691.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1440-1681.1993.tb01691.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,1417,23930,23931,25140,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4711099$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8324915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stokes, G. S.</creatorcontrib><creatorcontrib>Johnston, H. J.</creatorcontrib><creatorcontrib>Monaghan, J. C.</creatorcontrib><title>HUMORAL DETERMINANTS OF Na+ EXCRETION AFTER INTRAVENOUS NaCl LOADING IN NORMAL VOLUNTEERS</title><title>Clinical and experimental pharmacology & physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>SUMMARY
1. Twelve healthy volunteers maintained on a 100 mmol/day Na+ diet, were given an intravenous infusion of 2L saline (0.9%) between 10.00 and 13.00h on 2 study days at least 1 week apart. Urine collections (90 min) were made from 08.30 to 16.00 h. Either carbidopa 100 mg or indomethacin 50 mg was given orally at 07.45 h on one study day and placebo was given on the other (in random order).
2. On the placebo day, saline infusion caused significant decreases in plasma albumin concentration, plasma renin activity (PRA), plasma aldosterone concentration and urinary aldosterone excretion, with 2 to 3‐fold increases in plasma atrial natriuretic peptide (ANP) concentration and urinary dopamine: noradrenaline ratio (DA:NA), whereas mean urinary kallikrein and prostaglandin E2 (PGEI) excretion rates were unchanged. Carbidopa decreased urinary DA:NA and indomethacin decreased urinary PGE2 excretion, compared with the placebo day. Excretion of sodium (Na+) decreased below baseline in two out of six carbidopa‐treated subjects and in three out of six indomethacin‐treated subjects, but showed little or no change in the remainder.
3. These preliminary observations suggest that some subjects in the early phase of natriuresis after an intravenous Na+ load can be identified as having prostaglandin‐dependent or dopamine‐dependent mechanisms for Na+ excretion.</description><subject>Adolescent</subject><subject>Adult</subject><subject>aldosterone</subject><subject>Aldosterone - blood</subject><subject>Aldosterone - urine</subject><subject>Atrial Natriuretic Factor - blood</subject><subject>atrial natriuretic peptide</subject><subject>Biological and medical sciences</subject><subject>carbidopa</subject><subject>Carbidopa - administration & dosage</subject><subject>Carbidopa - pharmacology</subject><subject>Dopamine - urine</subject><subject>doparnine</subject><subject>excretion</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hemodynamics. Rheology</subject><subject>Humans</subject><subject>Indomethacin - administration & dosage</subject><subject>Indomethacin - pharmacology</subject><subject>indornethacin</subject><subject>kallikrein</subject><subject>Kallikreins - urine</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Na+</subject><subject>Natriuresis - drug effects</subject><subject>Norepinephrine - urine</subject><subject>prostaglandins</subject><subject>Prostaglandins - urine</subject><subject>Prostaglandins E - urine</subject><subject>renin</subject><subject>Renin - blood</subject><subject>Serum Albumin - analysis</subject><subject>Sodium - administration & dosage</subject><subject>Sodium - urine</subject><subject>Vertebrates: cardiovascular system</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkEFv0zAYhi0EGl3hJyBFCHFBCXbsOA6HSSFzu6DUgSQdcLLcxJFS0nWLW9H9exw16h1ffHje77W_B4D3CHrIns9bDxECXUQZ8lAUYe-wgYhGyDu9ALMLeglmEMPARSyEr8G1MVsIYQApvgJXDPskQsEM_L5br_IizpxbXvFilYpYVKWTLxyhPjn8V1LwKs2FEy8sdVJRFfE9F_m6tDzpnSyPb1OxtMARebGyNfd5thYV50X5BrxqVW_02-meg_WCV8mdm-XLNIkztyaYQrchOGwhrFufKBb6uGkQREHQ4IDBiCpCQo2YphhquolYo4giURS0EcWYhVRDPAcfz72Pw_7pqM1B7jpT675XD3p_NDIMGLFr-zb45Rysh70xg27l49Dt1PAsEZSjV7mVozw5ypOjVzl5lSc7_G565bjZ6eYyOom0_MPElalV3w7qoe7MJUZChKBtnIObc-xv1-vn__iATPh3jMZt3XNBZw76dClQwx9JQxwG8qdYyq8-K8sf2Up-w_8A942aiA</recordid><startdate>199305</startdate><enddate>199305</enddate><creator>Stokes, G. S.</creator><creator>Johnston, H. J.</creator><creator>Monaghan, J. C.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><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>199305</creationdate><title>HUMORAL DETERMINANTS OF Na+ EXCRETION AFTER INTRAVENOUS NaCl LOADING IN NORMAL VOLUNTEERS</title><author>Stokes, G. S. ; Johnston, H. J. ; Monaghan, J. C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4360-d437f00cf24a8723dd10155d358096a447e18e630e6b98da4a4995f9633876e03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>aldosterone</topic><topic>Aldosterone - blood</topic><topic>Aldosterone - urine</topic><topic>Atrial Natriuretic Factor - blood</topic><topic>atrial natriuretic peptide</topic><topic>Biological and medical sciences</topic><topic>carbidopa</topic><topic>Carbidopa - administration & dosage</topic><topic>Carbidopa - pharmacology</topic><topic>Dopamine - urine</topic><topic>doparnine</topic><topic>excretion</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hemodynamics. Rheology</topic><topic>Humans</topic><topic>Indomethacin - administration & dosage</topic><topic>Indomethacin - pharmacology</topic><topic>indornethacin</topic><topic>kallikrein</topic><topic>Kallikreins - urine</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Na+</topic><topic>Natriuresis - drug effects</topic><topic>Norepinephrine - urine</topic><topic>prostaglandins</topic><topic>Prostaglandins - urine</topic><topic>Prostaglandins E - urine</topic><topic>renin</topic><topic>Renin - blood</topic><topic>Serum Albumin - analysis</topic><topic>Sodium - administration & dosage</topic><topic>Sodium - urine</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stokes, G. S.</creatorcontrib><creatorcontrib>Johnston, H. J.</creatorcontrib><creatorcontrib>Monaghan, J. C.</creatorcontrib><collection>Istex</collection><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>Clinical and experimental pharmacology & physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stokes, G. S.</au><au>Johnston, H. J.</au><au>Monaghan, J. C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HUMORAL DETERMINANTS OF Na+ EXCRETION AFTER INTRAVENOUS NaCl LOADING IN NORMAL VOLUNTEERS</atitle><jtitle>Clinical and experimental pharmacology & physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>1993-05</date><risdate>1993</risdate><volume>20</volume><issue>5</issue><spage>310</spage><epage>312</epage><pages>310-312</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><coden>CEXPB9</coden><abstract>SUMMARY
1. Twelve healthy volunteers maintained on a 100 mmol/day Na+ diet, were given an intravenous infusion of 2L saline (0.9%) between 10.00 and 13.00h on 2 study days at least 1 week apart. Urine collections (90 min) were made from 08.30 to 16.00 h. Either carbidopa 100 mg or indomethacin 50 mg was given orally at 07.45 h on one study day and placebo was given on the other (in random order).
2. On the placebo day, saline infusion caused significant decreases in plasma albumin concentration, plasma renin activity (PRA), plasma aldosterone concentration and urinary aldosterone excretion, with 2 to 3‐fold increases in plasma atrial natriuretic peptide (ANP) concentration and urinary dopamine: noradrenaline ratio (DA:NA), whereas mean urinary kallikrein and prostaglandin E2 (PGEI) excretion rates were unchanged. Carbidopa decreased urinary DA:NA and indomethacin decreased urinary PGE2 excretion, compared with the placebo day. Excretion of sodium (Na+) decreased below baseline in two out of six carbidopa‐treated subjects and in three out of six indomethacin‐treated subjects, but showed little or no change in the remainder.
3. These preliminary observations suggest that some subjects in the early phase of natriuresis after an intravenous Na+ load can be identified as having prostaglandin‐dependent or dopamine‐dependent mechanisms for Na+ excretion.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>8324915</pmid><doi>10.1111/j.1440-1681.1993.tb01691.x</doi><tpages>3</tpages></addata></record> |
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| ispartof | Clinical and experimental pharmacology & physiology, 1993-05, Vol.20 (5), p.310-312 |
| issn | 0305-1870 1440-1681 |
| language | eng |
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| subjects | Adolescent Adult aldosterone Aldosterone - blood Aldosterone - urine Atrial Natriuretic Factor - blood atrial natriuretic peptide Biological and medical sciences carbidopa Carbidopa - administration & dosage Carbidopa - pharmacology Dopamine - urine doparnine excretion Female Fundamental and applied biological sciences. Psychology Hemodynamics. Rheology Humans Indomethacin - administration & dosage Indomethacin - pharmacology indornethacin kallikrein Kallikreins - urine Male Middle Aged Na+ Natriuresis - drug effects Norepinephrine - urine prostaglandins Prostaglandins - urine Prostaglandins E - urine renin Renin - blood Serum Albumin - analysis Sodium - administration & dosage Sodium - urine Vertebrates: cardiovascular system |
| title | HUMORAL DETERMINANTS OF Na+ EXCRETION AFTER INTRAVENOUS NaCl LOADING IN NORMAL VOLUNTEERS |
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