Article Figures & Data
Figures
- Figure 1.
Overview of the renin-angiotensin-aldosterone system (RAAS). The system has become increasingly complex with alternative ways of angiotensin II (AngII) formation besides angiotensin-converting enzyme (ACE; (Chymase, chymostatin-sensitive AngII-generating enzyme [CAGE]), a second form of ACE (ACE2), and novel peptides such as AngIV, angiotensin 1-9, and angiotensin 1-7. Clinically important could be that AngII can bind to AngII type 2 (AT2) receptors and AngIV to AT4 receptors that are not antagonized by sartanes, inducing proinflammatory and profibrotic effects (e.g., induction of chemokines, stimulation of plasminogen activator inhibitor-1).
- Figure 2.
Proximal tubular cells as an example of a local RAAS. Tubular cells could generate AngII in nanomolar concentrations and secrete into the tubular fluid as well as the interstitial space. Furthermore, tubular cells secrete intact angiotensinogen into the tubular fluid. Cells also could take renin and angiotensinogen up from the circulation, indicating a close interaction with the systemic RAAS. Although proximal tubular cells have ACE in their brush border membranes, it is controversial whether intracellular ACE contributes to AngII formation.
- Figure 3.
AngII is a cytokine with many effects on the kidney, clearly beyond the classical function as a hemodynamic mediator.
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