Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12958
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dc.contributor.authorHarrap, Stephen Ben
dc.contributor.authorDoyle, A Een
dc.date.accessioned2015-05-16T02:43:28Z
dc.date.available2015-05-16T02:43:28Z
dc.date.issued1988-01-01en
dc.identifier.citationClinical Science 1988; 74(1): 63-9en
dc.identifier.govdoc3276439en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12958en
dc.description.abstract1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from cross-breeding SHR and normotensive Wistar-Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherGlomerular Filtration Rateen
dc.subject.otherHemodynamicsen
dc.subject.otherHypertension.enzymology.genetics.physiopathologyen
dc.subject.otherKidney.physiopathologyen
dc.subject.otherMaleen
dc.subject.otherRatsen
dc.subject.otherRats, Inbred SHRen
dc.subject.otherRats, Inbred WKYen
dc.subject.otherRenal Circulationen
dc.subject.otherRenin.blooden
dc.titleGenetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat.en
dc.typeJournal Articleen
dc.identifier.journaltitleClinical Scienceen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pages63-9en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/3276439en
dc.type.austinJournal Articleen
item.grantfulltextnone-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
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