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Intrarenal angiotensin II and its contribution to the genesis of chronic hypertension Navar LG; Prieto MC; Satou R; Kobori HCurr Opin Pharmacol 2011[Apr]; 11 (2): 180-6The 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 AT(1) 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.|Angiotensin II/*physiology[MESH]|Angiotensinogen/physiology[MESH]|Animals[MESH]|Chronic Disease[MESH]|Humans[MESH]|Hypertension/*etiology[MESH]|Kidney Tubules, Collecting/physiology[MESH]|Kidney/*physiology[MESH]|Prorenin Receptor[MESH]|Receptors, Cell Surface/physiology[MESH]|Renin/physiology[MESH] |
