Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12873
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dc.contributor.authorJohnston, Colin Ien
dc.contributor.authorHodsman, G Pen
dc.contributor.authorHarrison, R Wen
dc.contributor.authorMendelsohn, Frederick AOen
dc.contributor.authorTsunoda, Ken
dc.date.accessioned2015-05-16T02:37:21Z
dc.date.available2015-05-16T02:37:21Z
dc.date.issued1988-03-11en
dc.identifier.citationThe American Journal of Medicine; 84(3A): 105-11en
dc.identifier.govdoc2851266en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12873en
dc.description.abstractPlasma atrial natriuretic peptide levels are increased in heart failure. In rats with experimental heart failure, the elevation in plasma atrial natriuretic peptide bore a close relationship to the size of the myocardial infarct and the degree of ventricular dysfunction. Sodium retention, assessed by changes in exchangeable body sodium, could not be demonstrated in this model of cardiac dysfunction. Even rats receiving a low-sodium diet had increased plasma atrial natriuretic peptide levels following coronary artery ligation despite a significant decrease in exchangeable body sodium. This establishes that the elevated plasma atrial natriuretic peptide levels found in heart failure are a consequence of ventricular dysfunction and increased intracardiac pressures rather than a reflection of the salt and water status. Alternatively, the elevated plasma atrial natriuretic peptide may limit salt and water retention in this model. In these animals with high circulating atrial natriuretic peptide levels, "down-regulation" of renal atrial natriuretic peptide receptors could be demonstrated. This decrease in renal atrial natriuretic peptide receptor numbers may, in part, explain the blunted response to infused atrial natriuretic peptide in heart failure. However, changes in renal atrial natriuretic peptide receptors alone would appear to be insufficient to lead to salt and water retention without the activation of other sodium-retaining mechanisms that occur with the progression of cardiac failure. Nevertheless, this down-regulation of renal atrial natriuretic peptide may then contribute to the salt and water retention that occurs in congestive biventricular heart failure. The close relationship between increases in atrial natriuretic peptide and ventricular dysfunction rather than sodium balance suggests that atrial natriuretic peptide's primary role in the circulation may be to produce venodilation and increase capillary permeability. This may act rapidly to reduce cardiac preload and prevent pulmonary congestion. Vasodilation and natriuresis may then become supplementary actions to maintain cardiac output and remove the excess fluid.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherAtrial Natriuretic Factor.blood.metabolism.physiologyen
dc.subject.otherHeart.physiopathologyen
dc.subject.otherHeart Failure.metabolism.pathology.physiopathologyen
dc.subject.otherKidney.metabolismen
dc.subject.otherMyocardium.pathologyen
dc.subject.otherRatsen
dc.subject.otherReceptors, Atrial Natriuretic Factoren
dc.subject.otherReceptors, Cell Surface.metabolismen
dc.subject.otherRenin.blooden
dc.subject.otherSodium.metabolismen
dc.titleRegulation of cardiac preload by atrial natriuretic peptide in congestive cardiac failure.en
dc.typeJournal Articleen
dc.identifier.journaltitleThe American journal of medicineen
dc.identifier.affiliationUniversity of Melbourne Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pages105-11en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/2851266en
dc.type.austinJournal Articleen
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
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