Renal oxidative stress, oxygenation and hypertension
2011 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 301, no 5, R1229-R1241 p.Article in journal (Refereed) Published
Hypertension is closely associated with progressive kidney dysfunction, manifested as glomerulosclerosis, interstitial fibrosis, proteinuria and eventually declining glomerular filtration. The postulated mechanism for development of glomerulosclerosis is barotrauma caused by increased capillary pressure, but the reason for development of interstitial fibrosis and the subsequently reduced kidney function is less clear. However, it has been hypothesized that tissue hypoxia induces fibrogenesis and progressive renal failure. This is very interesting, since recent reports highlight several different mechanisms resulting in altered oxygen handling and availability in the hypertensive kidney. Such mechanisms include decreased renal blood flow due to increased vascular tone induced by angiotensin II that limits oxygen delivery, increased oxidative stress resulting in increased mitochondrial oxygen usage, increased oxygen usage for tubular electrolyte transport and shunting of oxygen from arterial to venous blood in preglomerular vessels. It has been shown in several studies that interventions to prevent oxidative stress and to restore kidney tissue oxygenation prevent progression of kidney dysfunction. Furthermore, inhibition of angiotensin II activity, by either blocking AT(1)-receptors or angiotensin converting enzyme, or by preventing oxidative stress by administration of antioxidants also results in improved blood pressure control. It therefore seems likely that tissue hypoxia in the hypertensive kidney contributes to progression of kidney damage and perhaps also maintaining the high blood pressure.
Place, publisher, year, edition, pages
2011. Vol. 301, no 5, R1229-R1241 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-160916DOI: 10.1152/ajpregu.00720.2010ISI: 000296742100002PubMedID: 21832206OAI: oai:DiVA.org:uu-160916DiVA: diva2:453582