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Development of structural kidney damage in spontaneously hypertensive rats
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
2012 (English)In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 30, no 6, 1087-1091 p.Article, review/survey (Refereed) Published
Abstract [en]

The spontaneously hypertensive rat (SHR) is one of the major models of hypertension. This article describes the current state of knowledge about the mechanism behind kidney damage in SHR in the context of human hypertension and hypertensive kidney disease. It will argue that hypertensive damage in the SHR is pressure-dependent and shows how initial vascular damage leads to a loss of autoregulation and arterial hypertrophy in the juxtamedullary cortex while the outer cortical structures are relatively protected. Progressive arteriolar media hypertrophy then leads to the collapse of some glomeruli followed by tubular atrophy. The reduced glomerular filtration, thus, leads to compensatory hyperfiltration in another population of glomeruli which develop proteinuria and glomerulosclerosis. This model provides some important questions for future research. The regulation of media hypertrophy will be of great interest, as it might slow nephron loss and interstitial fibrosis. Finally, the mechanism by which reduced tubular flow leads to tubular atrophy is another important area for future research. Initial findings indicate that cilia activation may be of major importance for maintaining tubular structure.

Place, publisher, year, edition, pages
2012. Vol. 30, no 6, 1087-1091 p.
Keyword [en]
afferent arteriole, cilia, glomerulosclerosis, hypertension, kidney damage, media hypertrophy, nephrosclerosis, rat, spontaneously hypertensive rat, tubular atrophy
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-175532DOI: 10.1097/HJH.0b013e328352b89aISI: 000303933000005OAI: oai:DiVA.org:uu-175532DiVA: diva2:531961
Available from: 2012-06-08 Created: 2012-06-08 Last updated: 2017-12-07Bibliographically approved

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Hultström, Michael

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