ACEIs and ARBs cause compensatory rises in PRA
{"Image DocumentName": "ACEIs and ARBs cause compensatory rises in PRA", "Image ImageDescription": "Kidney. Glomerular vasoconstriction. Inflammation. Fibrosis. Angiotensinogen. Renin. Heart. Ang I. Hypertrophy. Fibrosis. Vasoconstriction. PRA. Non ACE pathways. ACE. Plasma renin activity (PRA) is a measure of the level of activity in the Renin System (RS) and is an indicator for hypertension. The RS is targeted at different places by existing antihypertensive therapies. Angiotensin converting enzyme (ACE) inhibitors or ACEIs reduce the production of angiotensin II (Ang II), by inhibiting the conversion of angiotensin I (Ang I) to Ang II by these enzymes. Angiotensin receptor blockers (ARBs) antagonize type 1 Ang II (AT1) receptors and prevent Ang II from binding. However, ACEIs and ARBs are associated with a feedback loop which increases PRA, as loss of stimulation of AT1 receptors on juxtaglomerular cells in the kidney (i.e. removal of negative feedback) leads to a compensatory increase in renin release. Diuretics also stimulate renin release, to activate the RS in response to a drop in fluid volume. The resulting increase in PRA may limit the organ protection offered by these drugs. Abbreviations. Ang I = angiotensin. ACE = angiotensin converting enzyme. ACEI = angiotensin converting enzyme inhibitor. ARB = angiotensin receptor blocker. AT1 = type 1 angiotensin II receptor. PRA = plasma renin activity. RS = Renin System. Reference. M\u00fcller DN, Luft FC. Direct renin inhibition with aliskiren in hypertension and target organ damage. Clin J Am Soc Nephrol 2006;1:221\u20138. ACEIs. Feedback Loop. Vessels. Ang II. Hyperplasia hypertrophy. Inflammation. Oxidation. Fibrosis. ARBs. AT1 Receptor. Brain. Biological effects. Vasoconstriction. Adapted from: M\u00fcller DN & Luft FC", "Image XResolution": "37", "Image YResolution": "37", "Image ResolutionUnit": "Pixels/Centimeter", "Image Software": "SlidePlayer", "Image YCbCrPositioning": "Centered"}