Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9596
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dc.contributor.authorHarrap, Stephen Ben
dc.date.accessioned2015-05-15T22:45:10Z
dc.date.available2015-05-15T22:45:10Z
dc.date.issued1992-05-16en
dc.identifier.citationClinical and Experimental Pharmacology & Physiology. Supplement; 19(): 19-22en
dc.identifier.govdoc1395112en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9596en
dc.description.abstract1. Certain genes drive the blood pressure of young spontaneously hypertensive rats (SHR) to stable hypertensive levels in adulthood. 2. Relatively brief blockade of the renin-angiotensin system in young SHR can reset the track of SHR pressure to a lower level for the life of the animal. This effect appears to be a characteristic of the SHR strain. 3. It is proposed that the expression of a particular SHR hypertensive gene depends on angiotensin and is limited to young animals. This hypothesis explains some of the phenotypic abnormalities observed in young SHR and the decremental long-term blood pressure effects following ACE inhibitor treatment. 4. The identity of the gene is unclear, but information from biochemical, physiological and pharmacological studies may direct attention to distinct candidate genes within specific chromosomal regions of interest. 5. Understanding these genetic mechanisms may have important implications for future preventive strategies.en
dc.language.isoenen
dc.subject.otherAging.physiologyen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherGene Expression.drug effectsen
dc.subject.otherHypertension.geneticsen
dc.subject.otherRatsen
dc.subject.otherRats, Inbred SHRen
dc.subject.otherRenin-Angiotensin System.drug effects.physiologyen
dc.titleA developmental genetic mechanism involving angiotensin in spontaneously hypertensive rats.en
dc.typeJournal Articleen
dc.identifier.journaltitleClinical and Experimental Pharmacology & Physiology. Supplementen
dc.identifier.affiliationDepartment of Medicine, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pages19-22en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/1395112en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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