Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12886
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dc.contributor.authorHodsman, G Pen
dc.contributor.authorKohzuki, Men
dc.contributor.authorHowes, L Gen
dc.contributor.authorSumithran, Een
dc.contributor.authorTsunoda, Ken
dc.contributor.authorJohnston, Colin Ien
dc.date.accessioned2015-05-16T02:38:12Z
dc.date.available2015-05-16T02:38:12Z
dc.date.issued1988-08-01en
dc.identifier.citationCirculation; 78(2): 376-81en
dc.identifier.govdoc2899463en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12886en
dc.description.abstractIn chronic cardiac failure, various neurohumoral mechanisms are activated to sustain blood volume, blood pressure, and organ perfusion. Using the coronary artery ligation model of heart failure in the rat, we have measured changes in vasoactive hormone secretion and related these changes to salt and water status during a 1-month period. When compared with controls, rats with infarction had a marked rise in plasma atrial natriuretic peptide (294 +/- 59 vs. 79 +/- 10 pg/ml, p less than 0.001) although there was no increase in total exchangeable body sodium. Plasma renin activity and plasma aldosterone concentrations were the same for both rats with infarction and controls. Similarly, there were no significant differences in plasma arginine vasopressin, plasma osmolality, or plasma sodium concentration in rats with infarction. Ventricular norepinephrine levels were reduced in animals with infarction (p less than 0.01). Plasma atrial natriuretic peptide levels were raised in this model of chronic left ventricular failure. However, there was no salt retention and little stimulation of the renin-angiotensin-aldosterone system or vasopressin. The results suggest that high circulating atrial natriuretic peptide levels may prevent or limit salt and water retention, either directly or indirectly, by inhibiting the renin-angiotensin-aldosterone system.en
dc.language.isoenen
dc.subject.otherAldosterone.blooden
dc.subject.otherAnimalsen
dc.subject.otherArginine Vasopressin.blooden
dc.subject.otherAtrial Natriuretic Factor.blooden
dc.subject.otherCatecholamines.metabolismen
dc.subject.otherChronic Diseaseen
dc.subject.otherFemaleen
dc.subject.otherIon Exchangeen
dc.subject.otherMyocardial Infarction.blood.metabolism.urineen
dc.subject.otherMyocardium.metabolismen
dc.subject.otherNeurotransmitter Agents.blood.metabolismen
dc.subject.otherOsmolar Concentrationen
dc.subject.otherRatsen
dc.subject.otherRats, Inbred Strainsen
dc.subject.otherRenin.blooden
dc.subject.otherSodium.blood.metabolismen
dc.titleNeurohumoral responses to chronic myocardial infarction in rats.en
dc.typeJournal Articleen
dc.identifier.journaltitleCirculationen
dc.identifier.affiliationUniversity of Melbourne Department of Medicine, Austin Hospital, Heidelberg, Australiaen
dc.description.pages376-81en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/2899463en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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