Intrarenal angiotensin II and its contribution to the genesis of chronic hypertension

The increased activity of intrarenal renin–angiotensin system (RAS) in a setting of elevated arterial pressure elicits renal vasoconstriction, increased sodium reabsorption, proliferation, fibrosis and renal injury. Increases in intrarenal and interstitial angiotensin (Ang) II levels are due to incr...

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Bibliographic Details
Published in:	Current opinion in pharmacology 2011-04, Vol.11 (2), p.180-186
Main Authors:	Navar, L Gabriel, Prieto, Minolfa C, Satou, Ryousuke, Kobori, Hiroyuki
Format:	Article
Language:	eng
Subjects:	Angiotensin II - physiology Angiotensinogen - physiology Animals Chronic Disease Humans Hypertension - etiology Internal Medicine Kidney - physiology Kidney Tubules, Collecting - physiology Medical Education Receptors, Cell Surface - physiology Renin - physiology
Online Access:	Get full text
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Summary:	The increased activity of intrarenal renin–angiotensin system (RAS) in a setting of elevated arterial pressure elicits renal vasoconstriction, increased sodium reabsorption, proliferation, fibrosis and renal injury. Increases in intrarenal and interstitial angiotensin (Ang) II levels are due to increased AT1 receptor mediated Ang II uptake and stimulation of renal angiotensinogen (AGT) mRNA and protein expression. Augmented proximal tubule AGT production increases tubular AGT secretion and spillover of AGT into the distal nephron and urine. Increased renin formation by principal cells of the collecting ducts forms Ang I from AGT thus increasing Ang II. The catalytic actions of renin and prorenin are enhanced by prorenin receptors (PRRs) on the intercalated cells. The resultant increased intrarenal Ang II levels contribute to the genesis of chronic hypertension.
ISSN:	1471-4892 1471-4973