Linked Life Data

11744766

Source:http://linkedlifedata.com/resource/pubmed/id/11744766

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 3
pubmed:dateCreated
2001-12-17
pubmed:abstractText
1. This study aims at determining whether elevation of renal perfusion pressure (RPP) may correct for increased total body sodium (TBS), via pressure natriuresis. 2. Freely moving dogs were studied on four consecutive days. During day 1, low-dose angiotensin II and aldosterone were infused. Pressure natriuresis was prevented by servo-controlling RPP to 20 % below the control level. Sodium and water retention increased TBS and total body water. Mean arterial blood pressure rose by approximately 25 mmHg. 3. In protocol 1, infusions and control of RPP were maintained over three more days. Sodium was retained on all days, resulting in a continuous increase in TBS. 4. In protocol 2, control of RPP was stopped after day 1. Thus, pressure natriuresis could exert its effect beginning with day 2. Angiotensin II and aldosterone infusions were continued. This prevented the effects of endogenous suppression of the renin-angiotensin-aldosterone system (RAAS), which is caused by increased TBS. No further sodium retention occurred, i.e. TBS remained at the elevated level gained on day 1. 5. In protocol 3, control of RPP and the infusions were stopped. Thus, pressure natriuresis and RAAS suppression could exert their combined effects. Sodium excretion exceeded sodium intake on day 2. Control level of TBS was regained within 24 h. 6. It was concluded that when RPP is considerably elevated, pressure natriuresis prevents further increase of TBS in the face of elevated angiotensin II and aldosterone levels. However, pressure natriuresis does not suffice to restore TBS to control. This requires additional endogenous suppression of RAAS.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-10444563, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-1480667, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-1731371, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-1733305, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-2063193, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-2217555, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-2240271, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-6720967, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-6724669, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-7573546, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-8141366, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-8964947, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-9004086, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-9277550, http://linkedlifedata.com/resource/pubmed/commentcorrection/11744766-9428620
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
537
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
941-7
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Contribution of pressure natriuresis to control of total body sodium: balance studies in freely moving dogs.
pubmed:affiliation
Institut für Physiologie, Universitätsklinikum Charité, Humboldt-Universität zu Berlin, Germany. erdmann.seeliger@charite.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't