Intrarenal Angiotensin II Augmentation in Hypertension
Angiotensin (Ang) II-dependent hypertension is characterized by an augmentation in intrarenal Ang II content beyond circulating levels that is associated with functional and morphological derangements in the kidney. This augmentation is due to Ang II sequestration from the general circulation by the Ang II type 1 receptor (AT1R) and to intrarenal Ang II formation by a local renin–angiotensin system (RAS). This review summarizes the evidence in favor of the contribution of these two processes to the observed augmentation of intrarenal Angiotensin II as well as their impact on the regulation of kidney function and blood pressure regulation.
KeywordsHigh Performance Liquid Chromatography Filtration Angiotensin Luminal Renin
This work was supported by grants from the Institutional Award (IDeA) program of NCRR (P20RR017659), the National Heart, Lung, and Blood Institute (HL26371), the National Institute of Diabetes and Digestive and Kidney Diseases (DK072408) and a postdcotoral fellowship from the Consortium for Southeastern Hypertension Control.
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